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1.
Article in Chinese | WPRIM | ID: wpr-1028731

ABSTRACT

AIM To explore the effects of Shiquan Dabu Decoction on the synaptic function and cognitive impairment in a mouse model of Alzheimer's disease(AD).METHODS Sixty mice were randomly divided into the control group,the model group,the memantine group(5 mg/kg)and the high,medium and low dose Shiquan Dabu Decoction groups(6.24,3.12 and 1.56 g/kg),with 10 mice in each group.Except for those of the control group,the mice of other groups underwent their 70-day AD models induction by intraperitoneal injection of D-galactose and gavage feeding of AlCl3,followed by 42-day corresponding dosing of drugs by gavage on the 29th day.The mice had their spatial learning and associative memory detected by Morris water maze test and conditioned fear test;their morphological changes of hippocampal neurons observed by HE staining;their serum SOD activity,MDA level,and SOD,AChE activities and MDA,ACh,TNF-α and IL-1β levels in hippocampus detected by kits;and their PSD-95,Shank3,NR1,NR2A,NR2B,AMPK and p-AMPK protein expressions in hippocampus detected by Western blot.RESULTS Compared with the model group,the high-dose Shiquan Dabu Decoction group displayed improved spatial learning and memory ability and associative memory(P<0.05,P<0.01);reduced pathological damage of hippocampal neurons,decreased levels of oxidative stress and inflammation(P<0.05,P<0.01);enhanced cholinergic transmission(P<0.05,P<0.01),and increased protein expressions of PSD-95,Shank3,NR1,NR2A,NR2B,and p-AMPK in hippocampal tissue(P<0.05,P<0.01).CONCLUSION Shiquan Dabu Decoction can improve the cognitive impairment of in the mouse model of AD,and its mechanism may be related to AMPK activation and synaptic function restoration.

2.
Article in Chinese | WPRIM | ID: wpr-1019090

ABSTRACT

Active physical exercise can effectively alleviate the pathological process of chronic cerebral ischemia(CCH)and improve learning and memory ability.This paper reviews the possible biological mechanisms of aerobic exercise to delay the pathological process of chronic cerebral ischemia and improve learning and memory.Previous studies have found that aerobic exercise can improve the neuroprotective effect,enhance the plasticity of hippocampal synapses,improve the activity of the upper and lower pathways of hippocampal tissue,and improve learning and memory ability.However,the intervention effect of aerobic exercise on chronic cerebral ischemia should be fully considered at the intervention time,and the intervention effect is also different.

3.
Article in Chinese | WPRIM | ID: wpr-1021507

ABSTRACT

BACKGROUND:Exercise improves Alzheimer's disease,dementia,and age-related cognitive abilities.A potential mediator between exercise and these health benefits may be adult hippocampal neurogenesis.Therefore,it is of great significance to explore whether and how exercise affects the adult hippocampal neurogenesis process in Alzheimer's disease mice. OBJECTIVE:To observe the effect of aerobic exercise on adult hippocampal neurogenesis of Alzheimer's disease mice,and to explore whether aerobic exercise can promote their adult hippocampal neurogenesis. METHODS:Three-month-old wild-type(C57BL/6Jnju)and APP/PS1 double transgenic Alzheimer's disease mice were randomly divided into four groups:wild control group,wild exercise group,Alzheimer's disease control group and Alzheimer's disease exercise group,with 20 mice in each group.The control group did not do exercise,and the exercise group did aerobic exercise for 5 months.After exercise intervention,real-time PCR,immunofluorescence and western blot assay were used to detect the expression levels of DCX,Ki67,βIII-tubulin and NeuN in the hippocampal tissue of mice in each group. RESULTS AND CONCLUSION:The expressions of DCX,βIII-tubulin and NeuN in the hippocampal dentate gyrus in the Alzheimer's disease control group were significantly lower than those in the wild control group(P<0.05).The expressions of DCX,Ki67,βIII-tubulin and NeuN were significantly higher in the hippocampal dentate gyrus in the Alzheimer's disease exercise group than those in the Alzheimer's disease control group(P<0.05).It is indicated that long-term aerobic exercise intervention can strengthen the proliferation,migration and differentiation of neurons during adult hippocampal neurogenesis and significantly increase the number of neuronal precursor cells and new neurons in Alzheimer's disease mice.

4.
Article in Chinese | WPRIM | ID: wpr-1021820

ABSTRACT

BACKGROUND:β-amyloid protein and Tau protein have adverse effects on the cognitive function of Alzheimer's disease patients,and Notch1 and Caspase-3 can regulate the expression of β-amyloid protein and Tau protein.It is not clear whether Notch1 and Caspase-3 mediate the process of aerobic exercise to improve the cognitive ability of Alzheimer's disease patients.At present,there is a lack of studies on the effect of long-term aerobic exercise on the expression of Notch1 and Caspase-3 in the hippocampus of Alzheimer's disease mice. OBJECTIVE:To observe the expression of Notch1 and Caspase-3 in the hippocampus of Alzheimer's disease mice undergoing long-term aerobic exercise and to investigate the effects of Notch1 and Caspase-3 in Alzheimer's disease mice. METHODS:Wild type and APP/PS1 double-transgenic Alzheimer's disease mice aged 3 months were randomly divided into four groups:wild control group,wild exercise group,Alzheimer's disease control group and Alzheimer's disease exercise group,with 20 mice in each group.Mice in the control groups were not subjected to exercise,while those in the exercise groups received aerobic exercise intervention for 5 months.After the exercise intervention,Morris water maze was used to detect the spatial learning and memory ability of mice.Real-time PCR,immunofluorescence and western blot were used to detect the expressions of Aβ1-42,Tau,Notch1 and Caspase-3 in the hippocampal tissues of mice in each group. RESULTS AND CONCLUSION:The spatial learning and memory ability of Alzheimer's mice was significantly worse than that of wild-type mice(P<0.05).The spatial learning and memory ability of mice in the exercise groups were significantly better than that in the corresponding control groups(P<0.05).The expressions of Aβ1-42,Tau,Notch1 and Caspase-3 in the hippocampus were significantly higher in the Alzheimer's disease control group than the wild control group(P<0.05)and were significantly lower in the Alzheimer's disease exercise group than the Alzheimer's disease control group(P<0.05).To conclude,long-term aerobic exercise can improve the spatial learning and memory ability of Alzheimer's disease mice,which may be related to the decreased expression of Notch1,Caspase-3,Aβ1-42 and Tau protein in the hippocampus of Alzheimer's disease mice.

5.
Article in Chinese | WPRIM | ID: wpr-973652

ABSTRACT

Background Formaldehyde and benzene homologues are common environmental pollutants, and their neurotoxicity has aroused widespread concern. Objective To investigate the effect of taurine on cognitive impairment after exposure to formaldehyde and benzene analogues in young rats. Methods Twenty four-week old SD rats were randomly divided into four groups, with six rats in each group: control group (clean air), model group (5 mg·m−3 formaldehyde + 5 mg·m−3 benzene + 10 mg·m−3 toluene + 10 mg·m−3 xylene), low-dose taurine intervention group (5 g·L−1 taurine + mixture of formaldehyde and benzene analogues), and high-dose taurine intervention group (10 g·L−1 taurine + formaldehyde and mixture of benzene analogues), and the exposure was administered by oral and nasal aerosol inhalation for 28 d. At the end of exposure, the learning and memory ability of rats in each group was measured by Morris water maze test. After the behavioral test, the rats were anesthetized and neutralized, and the brain tissue was harvested for histopathological and molecular biological tests. The apoptosis rate of neurons in hippocampal CA1 area was detected by Tunel assay, and the expression levels of apoptosis-related proteins such as caspase 3, bax, and bcl-2 in hippocampal tissue were detected by Western blotting. Results The growth and development of rats in each group were good during inhalation. During the Morris water maze experiment, the escape latencies of rats in the taurine intervention groups were not different from that in the control group (P>0.05) from day 3 to day 5 of training, while the escape latency of rats in the model group was significantly higher than that in the control group (P <0.05). The number of crossing platform and the target quadrant residence time in the high-dose taurine intervention group were not different from those in the control group (P>0.05), while the two variables in the model group and low-dose taurine intervention group were significantly lower than those in the control group (P <0.05). The apoptotic rates of neurons in the hippocampal CA1 area of rats in the control group, model group, and low-dose and high-dose taurine intervention groups were 5.11%, 18.87%, 9.39%, and 4.63%, respectively. The apoptotic rate in the model group was higher than those in the control group and low-dose and high-dose taurine intervention groups (P<0.05). The expression levels of caspase 3, bax, and bcl-2 in the hippocampus of rats in the low-dose and high-dose taurine intervention groups showed no difference compared with the control group (P>0.05). The expression levels of caspase 3 and bax in the model group were higher than those in the control group and low-dose or high-dose taurine intervention groups (P<0.05), and the expression levels of bcl-2 was lower (P<0.05). Conclusion The mixed exposure to formaldehyde and benzene analogues can damage the learning and memory ability of young rats, and increase the apoptosis of neurons in hippocampal CA1 region. Taurine can reverse the damage induced by formaldehyde and benzene analogues.

6.
Zhongguo zhenjiu ; (12): 800-806, 2023.
Article in Chinese | WPRIM | ID: wpr-980798

ABSTRACT

OBJECTIVE@#To observe the effects of moxa smoke through olfactory pathway on learning and memory ability in rapid aging (SAMP8) mice, and to explore the action pathway of moxa smoke.@*METHODS@#Forty-eight six-month-old male SAMP8 mice were randomly divided into a model group, an olfactory dysfunction group, a moxa smoke group and an olfactory dysfunction + moxa smoke group, with 12 mice in each group. Twelve age-matched male SAMR1 mice were used as the blank group. The olfactory dysfunction model was induced in the olfactory dysfunction group and the olfactory dysfunction + moxa smoke group by intraperitoneal injection of 3-methylindole (3-MI) with 300 mg/kg, and the moxa smoke group and the olfactory dysfunction + moxa smoke group were intervened with moxa smoke at a concentration of 10-15 mg/m3 for 30 min per day, with a total of 6 interventions per week. After 6 weeks, the emotion and cognitive function of mice was tested by open field test and Morris water maze test, and the neuronal morphology in the CAI area of the hippocampus was observed by HE staining. The contents of neurotransmitters (glutamic acid [Glu], gamma-aminobutyric acid [GABA], dopamine [DA], and 5-hydroxytryptamine [5-HT]) in hippocampal tissue of mice were detected by ELISA.@*RESULTS@#The mice in the blank group, the model group and the moxa smoke group could find the buried food pellets within 300 s, while the mice in the olfactory dysfunction group and the olfactory dysfunction + moxa smoke group took more than 300 s to find them. Compared with the blank group, the model group had increased vertical and horizontal movements (P<0.05) and reduced central area residence time (P<0.05) in the open field test, prolonged mean escape latency on days 1-4 (P<0.05), and decreased search time, swimming distance and swimming distance ratio in the target quadrant of the Morris water maze test, and decreased GABA, DA and 5-HT contents (P<0.05, P<0.01) and increased Glu content (P<0.05) in hippocampal tissue. Compared with the model group, the olfactory dysfunction group had increased vertical movements (P<0.05), reduced central area residence time (P<0.05), and increased DA content in hippocampal tissue (P<0.05); the olfactory dysfunction + moxa smoke group had shortened mean escape latency on days 3 and 4 of the Morris water maze test (P<0.05) and increased DA content in hippocampal tissue (P<0.05); the moxa smoke group had prolonged search time in the target quadrant (P<0.05) and increased swimming distance ratio, and increased DA and 5-HT contents in hippocampal tissue (P<0.05, P<0.01) and decreased Glu content in hippocampal tissue (P<0.05). Compared with the olfactory dysfunction group, the olfactory dysfunction + moxa smoke group showed a shortened mean escape latency on day 4 of the Morris water maze test (P<0.05). Compared with the moxa smoke group, the olfactory dysfunction + moxa smoke group had a decreased 5-HT content in the hippocampus (P<0.05). Compared with the blank group, the model group showed a reduced number of neurons in the CA1 area of the hippocampus with a disordered arrangement; the olfactory dysfunction group had similar neuronal morphology in the CA1 area of the hippocampus to the model group. Compared with the model group, the moxa smoke group had an increased number of neurons in the CA1 area of the hippocampus that were more densely packed. Compared with the moxa smoke group, the olfactory dysfunction + moxa smoke group had a reduced number of neurons in the CA1 area of the hippocampus, with the extent between that of the moxa smoke group and the olfactory dysfunction group.@*CONCLUSION@#The moxa smoke could regulate the contents of neurotransmitters Glu, DA and 5-HT in hippocampal tissue through olfactory pathway to improve the learning and memory ability of SAMP8 mice, and the olfactory is not the only effective pathway.


Subject(s)
Male , Animals , Mice , Olfactory Pathways , Smoke/adverse effects , Serotonin , Aging , Dopamine , Olfaction Disorders/etiology
7.
Article in Chinese | WPRIM | ID: wpr-931938

ABSTRACT

Objective:To investigate the effect of activation of microglia in prefrontal cortex on long-term spatial memory in post-stroke depression mice.Methods:Forty-eight male C57BL/6 mice were divided into sham operation group, stroke group, post-stroke depression group and depression group according to the random number table method with 12 in each group, and 36 mice were divided into solvent group, enrofloxacin group and minocycline group according to the random number table method with 12 in each group.Middle cerebral artery occlusion (MCAO) was use to establish the stroke model, and forced swimming was used to establish the depression model.The post-stroke depression model mice were received MCAO first and then received forced swimming on the 4th day after stroke to establish the model.Mice in enrofloxacin group and minocycline group were treated with enrofloxacin and minocycline injection once a clay for 14 days from the 5th day after stroke, respectively.Forced swimming test and sugar water preference test were used to evaluate the depression of mice in each group, Morris water maze test was used to detect the spatial memory function of mice in each group, and Nissl staining and immunofluorescence staining were used to detect the neuronal function and the number and type of microglia activation.The expression of inflammatory cytokines IL-6 and IL-1β were detected by Western blot.GraphPad Prism 8.0.1 statistical software was used for statistical analysis.The single factor variance analysis was used to compare the difference among multiple groups, and pairwise comparison was performed with SNK- q test. Results:(1) There were statistically significant differences in depression, learning and memory, neuron damage, activation of microglia, inflammatory factors and other indicators in sham operation group, stroke group, post-stroke depression group and depression group ( F=43.58-255.70, all P<0.05). Compared with stroke group, post-stroke depression group had longer floating immobility time ((222.70±29.12) s, (79.25±46.78) s, P<0.05), the preference rate of sugar water was significantly lower ( (49.44±6.19) %, (84.49±4.73) %, P<0.05), and the average value of platform approach after correction was higher((125.00±9.95) mm, (96.79±12.57) mm, P<0.05), Nissl bodies expression was lower ((53.50±15.78) cells /mm 2, (85.67±17.52) cells /mm 2, P<0.05), NeuN positive expression rate was lower ((29.78±3.70) %, (45.73±4.51) %, P<0.05), the percent of M1 microglia expression was significantly higher ((75.55±8.84) %, (58.19±5.69) %, P<0.05), the percent of M2 microglia expression was lower ((43.46±5.11)%, (57.14±5.40)%, P<0.05), and the expression levels of IL-6 ((1.14±0.03), (0.94±0.05), P<0.05) and IL-1β((1.17±0.03), (0.56±0.04), P<0.05) were significantly higher.(2) Depression, learning and memory, neuron injury, activation of microglia, inflammatory factors and other indicators of mice in solvent group, enrofloxacin group and minocycline group were significantly different ( F=7.13-94.35, all P<0.05). Compared with enrofloxacin group, mice in minocycline group had shorter floating immobility time ((169.30±13.04) s, (224.30±22.60) s, P<0.05) and higher sugar water preference rate ((62.81±7.75) %, (47.71±8.11) %, P<0.05), the mean value of platform approach estimation after water maze correction was lower ((97.66±14.56) mm, (120.20±12.08) mm, P<0.05), and the expression level of Nissl bodies was higher ((80.17±10.55) cells /mm 2, (52.00±8.94) cells /mm 2, P<0.05), NeuN expression rate was high ((45.04±3.62) %, (28.88±4.50) %, P<0.05), Iba-1 expression was lower ((97.33±10.67) cells/mm 2, (112.50±6.54)cells/mm 2, P<0.05), the percent of M1 microglia expression was lower ((54.43±5.22) %, (73.82±6.88) %, P<0.05), and the percent of M2 microglia expression was significantly higher ((51.86±6.22) %, (36.30±5.72) %, P<0.05). The expression levels of IL-6 ((0.75±0.06), (1.21±0.07), P<0.05) and IL-1β ((0.61±0.06) (1.09±0.09), P<0.05) were lower. Conclusion:The long-term spatial memory impairment of post-stroke depression mice is aggravated, which is related to the neuron damage caused by increased activation of M1 microglia in PFC area.Inhibition of M1 microglia by minocycline can effectively improve the spatial memory ability of mice.

8.
Article in Chinese | WPRIM | ID: wpr-960484

ABSTRACT

Background The altered expressions of hippocampal N-methyl-D-aspartate (NMDA) receptors induced by benzo[ɑ]pyrene (BaP) causes short-term spatial learning and memory impairment in humans and animals, but whether BaP causes alterations of NMDA receptor subunits in other brain regions and the associated neurotoxic mechanism is still essentially unknown. Objective To observe the mRNA expressions of NR1, NR2A, and NR2B of NMDA receptor subunits in different brain regions in SD rat model with subchronic exposure to BaP, and to provide a basis for in-depth study of the mechanism of BaP-induced neurotoxicity. Methods Forty male SD rats were selected and randomly divided into a control group and 1.00, 2.50, and 6.25 mg·kg−1 BaP exposure groups with 10 rats in each group. The exposure rats received intraperitoneal injection of BaP every other day for 90 d.The average latency to platform, the average total distance, and the duration spent in previous quadrant were measured by the Morris Water Maze. Real-time fluorescence quantitative PCR was used to detect the mRNA expressions of NR1, NR2A, and NR2B in hippocampus, cortex, cerebellum, and striatum of rats. Results The average latency to platform and the average total distance in the 2.50 and 6.25 mg·kg−1 BaP groups were significantly prolonged compared with the control group (P<0.05), and the duration that rats spent in previous quadrant in the 6.25 mg·kg−1 BaP group was significantly shortened (P<0.05). Compared with the control group, the mRNA expressions of NR1 and NR2B in the hippocampus in the 2.50 and 6.25 mg·kg−1 BaP groups were significantly reduced (P<0.05), and the NR2A mRNA expression in the hippocampus in the 6.25 mg·kg−1 BaP group was significantly reduced (P<0.05); the mRNA expressions of NR1 and NR2B in the cortical tissue in the 6.25 mg·kg−1 BaP group were significantly reduced (P<0.05), and the mRNA expression of NR2A in the cortical tissue in the 1.00 mg·kg−1 BaP group was reduced; the mRNA expression of NR2B in the cerebellar tissue in the 6.25 mg·kg−1 BaP group was significantly reduced (P<0.05); there were no differences in the mRNA expressions of NMDA receptor subunits in the striatum tissue (P>0.05). Conclusion Subchronic BaP exposure can cause short-term spatial learning and memory impairment in rats, which may be related to the down-regulation of mRNA expressions of NR1, NR2A, and NR2B in hippocampus, changes of mRNA expressions of NR1, NR2A, and NR2B in cortical area, and the down-regulation of NR2B mRNA expression in cerebellum.

9.
Article in Chinese | WPRIM | ID: wpr-906076

ABSTRACT

Objective:To explore the underlying protective mechanism of Kaixinsan on learning, memory, and synaptic function in APP/PS1 mice. Method:Sixty APP/PS1 mice were randomly divided into a model group, a donepezil (2 mg·kg<sup>-1</sup>·d<sup>-1</sup>) group, and low- (0.7 g·kg<sup>-1</sup>·d<sup>-1</sup>), medium- (1.4 g·kg<sup>-1</sup>·d<sup>-1</sup>), and high-dose (2.8 g·kg<sup>-1</sup>·d<sup>-1</sup>) Kaixinsan groups, and the wild-type mice of the same age in the same litter were assigned to the normal group, with 12 mice in each group. After continuous intragastric administration for two months, the Morris water maze experiment was performed. The ultrastructure of hippocampal neurons was observed by transmission electron microscopy. The colorimetric assay was used to detect serum content of acetylcholine (ACh), choline acetyltransferase (ChAT), acetylcholinesterase (AChE), and levels of hippocampal reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px). Real-time fluorescence-based quantitative polymerase chain reaction (Real- time PCR) was used to detect the mRNA expression of hippocampal brain-derived neurotrophic factor (BDNF), beta-nerve growth factor (NGFB), discs large homolog (DLG)2, DLG4, and synaptophysin (SYP). Result:Compared with the normal group, the model group showed prolonged escape latency, reduced number of crossing platforms, shortened stay in the target quadrant (<italic>P</italic><0.01), decreased number of mitochondria with different shapes and irregular arrangement, some swollen and deformed mitochondria with broken mitochondrial cristae, endolysis, and cytoplasm vacuole, and more cell debris. Additionally, the model group also displayed reduced serum levels of ACh and ChAT, increased AChE (<italic>P</italic><0.01), elevated hippocampal ROS and MDA (<italic>P</italic><0.05,<italic>P</italic><0.01), declining SOD and GSH-Px (<italic>P</italic><0.01), and diminished hippocampal BDNF, NGFB, DLG2, DLG4, and SYP mRNA levels (<italic>P</italic><0.05,<italic>P</italic><0.01). Compared with the model group, the donepezil group, and the medium- and high-dose Kaixinsan groups showed shortened escape latency, increased number of crossing platforms, prolonged stay in the target quadrant (<italic>P</italic><0.05,<italic>P</italic><0.01), improved mitochondrial damage with a regular shape (mainly oval shape), relieved mitochondrial swelling and deformation, and clear mitochondrial cristae. Furthermore, the donepezil group, and the medium- and high-dose Kaixinsan groups also exhibited increased serum ACh and ChAT levels (<italic>P</italic><0.05,<italic>P</italic><0.01), blunted AChE activity (<italic>P</italic><0.05), reduced hippocampal ROS level (<italic>P</italic><0.05,<italic>P</italic><0.01), declining MDA level (<italic>P</italic><0.05), potentiated SOD and GSH-Px activities, and up-regulated hippocampal BDNF, NGFB, DLG2, DLG4, and SYP mRNA levels (<italic>P</italic><0.05,<italic>P</italic><0.01). In the low-dose Kaixinsan group, the stay time in the target quadrant was prolonged and the expression of hippocampal SYP mRNA was elevated significantly (<italic>P</italic><0.05). There was no statistical difference in swimming speed between the groups. Conclusion:Kaixinsan can improve the learning and memory ability of APP/PS1 mice by increasing the expression of synaptic plasticity-related proteins, reducing the ultrastructural damage to hippocampal neurons, resisting oxidative stress, and regulating cholinergic neurotransmitters, thereby exerting neuroprotective effects.

10.
Article in Chinese | WPRIM | ID: wpr-906105

ABSTRACT

Objective:To observe the effect of Shengyutang on the levels of monoamine neurotransmitters in the hippocampus, and explore its possible mechanism on improving the learning and memory abilities of sleep deprivation (SD) mice. Method:The 50 mice were divided into normal group, model group, estazolam group, Shengyutang low and high dose groups, with 10 mice in each group. A multi-platform water environment was used to prepare SD mouse models. The low and high-dose Shengyutang groups received intragastric administration of 12.5, 25 g·kg<sup>-1</sup>, respectively. The mice in the model group were intragastrically administered with the same dose of normal saline daily for 8 weeks. Morris water maze experiment was used to observe the behavioral changes of SD mice in the evasion latency period, the number of crossing platforms, and the stay time in the target quadrant of each group. HE staining was used to observe the pathomorphological changes of the hippocampal tissue of each group. The expression levels of eight monoamine neurotransmitters including serotonin (5-HT),dopandne (DA),epinephrine (EP),norepinephrine (NE),5-hydroxyindole acetic acid(5-HIAA), high vanillic acid (HVA), levodopa(<italic>L</italic>-DOPA),and 3,4-dihydroxyphenylacetic acid(DOPAC)were detected by high performance liquid chromatography, and the expression levels of c-Fos protein in hippocampus were detected by immunohistochemistry. Result:Compared with the normal group, the SD mice in the model group were in a poorer general state and severe fatigue was observed. Compared with the model group, SD mice in each dose group of Shengyutang got improved in eating, activity, sleep, hair color, and response to external stimuli. Compared with the normal group, the body weight of SD mice in the model group was significantly reduced (<italic>P</italic><0.05), but the body weight in the Shengyutang high-dose group increased the most as compared with the model group (<italic>P</italic><0.05). Compared with the normal group, the hippocampal cells in the model group were disorderly arranged, incomplete in shape, increased in gap and decreased in number. Compared with the model group, the number of neurons in the hippocampus of SD mice in each dose group of Shengyutang increased. Compared with the normal group, the escape latency time of SD mice in the model group was significantly prolonged, the times of crossing platform and the residence time in the target quadrant significantly decreased (<italic>P</italic><0.01). Compared with the model group, the times of crossing platform and the residence time in the target quadrant of mice in each dose group of Shengyutang significantly increased (<italic>P</italic><0.05, <italic>P</italic><0.01). Compared with the normal group, the levels of 5-HT, 5-HIAA, <italic>L</italic>-DOPA, DOPAC, EP, NE, HVA and DA in the model group significantly decreased (<italic>P</italic><0.05,<italic> P</italic><0.01); but these levels in each dose group of Shengyutang were higher than those in model group (<italic>P</italic><0.05). Compared with the normal group, the average MD value of c-Fos protein in the hippocampus of the model group significantly increased (<italic>P</italic><0.01), and the expression levels of c-Fos protein in the hippocampus of Shengyutang groups were significantly lower than those in model group (<italic>P</italic><0.01). Conclusion:Shengyutang can improve the learning and memory abilities of SD rats, and its mechanism may be related to the decrease of monoamine neurotransmitter and c-Fos protein expression.

11.
Acupuncture Research ; (6): 617-622, 2020.
Article in Chinese | WPRIM | ID: wpr-844111

ABSTRACT

OBJECTIVE: To compare the effect of electroacupuncture (EA) of acupoint group for "reinforcing the kidney and regulating Governor Vessel" and acopoint group for "reinforcing the kidney and lung and regulating Governor Vessel" on lear-ning-memory ability and expression of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) proteins in the hippocampus and prefrontal cortex (PFC) in Alzheimer's disease (AD) rats, so as to explore the efficacy of the two acupoint groups and mechanisms underlying improvement of AD. METHODS: Forty male SD rats were randomly divided into control, sham operation, model, "Baihui" + "Shenshu" (GV20+BL23, for "reinforcing the kidney and regulating Governor Vessel") EA and GV20+BL23+ "Feishu" (BL13, GV20+BL23+BL13, for "reinforcing the kidney and lung and regulating Governor Vessel") EA groups (n=8 rats in each group). The AD model was established by bilateral injection of amyloid β peptide (Aβ25-35,10 μL) into bilateral hippocampus, and rats of the sham operation group received injection of normal saline. After successful establishment of the model,EA (2 Hz, 2 mA) was applied to these acupoints for 15 min, once daily for 10 days. Then, the learning-memory ability was assessed by using Morris water maze tests, and the expression levels of TNF-α and IL-1β proteins in the PFC and hippocampus tissues were detected by using Western blot. RESULTS: Following modeling, the average escape latency of place navigation test were significantly increased (P0.05). CONCLUSION: EA of both GV20+BL23 and GV20+BL23+BL13 acupoint can improve learning-memory ability of AD rats, which is associated with their effects in down-regulating the expression of IL-1β and TNF-α in the PFC and hippocampus to reduce inflammatory reaction. There were no significant differences between the two acupoint groups in the therapeutic effects.

12.
Acupuncture Research ; (6): 611-616, 2020.
Article in Chinese | WPRIM | ID: wpr-844118

ABSTRACT

OBJECTIVE: To investigate the effect of electroacupuncture (EA) at "Baihui"(GV20), "Fengfu"(GV16) and bilateral "Shenshu"(BL23) on learning-memory ability, apoptosis in the hippocampus and expression of Aβ, Caspase 3, Bax and Bcl-2 proteins in the hippocampus and cerebral cortex in immature mice with Alzheimer's disease (AD), so as to explore its mechanism underlying improvement of AD. METHODS: Forty APP/PS1 transgenic male young mice were equally randomized into model and EA groups and 20 C57BL/6J male young mice were used as the normal control. EA (10 Hz, about 2 mA) was applied to GV20-BL23 and GV16-BL23 for 20 min, once daily, 6 days a week for 16 weeks. The Morris water maze swimming test was used to evaluate the animals' learning-memory ability. Congo red staining and immunohistochemical staining were used to detect senile plaques in the hippocampus (dentate gyrus) and cerebral cortex tissues. Terminal deoxynucleotidyl transferase-mediated dUTP Nick-end Labeling (TUNEL) was used to detect the cellular apoptosis of hippocampus. The expression levels of apoptosis related factors Caspase 3, Bax and Bcl-2 were detected by Western blot. RESULTS: After modeling, the escape latency of place navigation test of Morris water maze swimming tasks was significantly increased (P0.05). CONCLUSION: EA of GV20, GV16 and BL23 can effectively improve the learning-memory ability in AD mice, which may be related to its function in inhibiting neuronal apoptosis in the hippocampus and down-regulating the expression levels of Aβ, Caspase 3 and Bax proteins in both hippocampus and cerebral cortex.

13.
Acupuncture Research ; (6): 529-534, 2020.
Article in Chinese | WPRIM | ID: wpr-844138

ABSTRACT

OBJECTIVE: To observe the effect of electroacupuncture (EA) and manual acupuncture (MA) on learning-memory ability, changes of ultrastructure of neurons and expression of CDK5 and Tau proteins in hippocampus of SAMP8 mice,so as to explore its mechanisms underlying improvement of Alzheimer's disease (AD).. METHODS: A total of 45 male SAMP8 mice were randomly divided into model, EA and MA groups, with 15 mice in each group. The other 15 SAMR1 mice were used as the normal group. In the EA group, EA (2 Hz, 1 mA) was applied to bilateral "Shenshu"(BL23) and manual acupuncture was applied to "Baihui"(GV20) for 20 min. In the MA group, MA was applied to GV20 and bilateral BL23 for 20 min. Both group were treated once a day for 31 days, and with an interval of one day between every two 7 days. Morris water maze was performed to assess the animals' learning-memory ability. The morphological changes of hippocampal neurons were observed under transmission electron microscopy. The expression levels of CDK5, p25 and Tau-5 proteins in the hippocampus were detected by immunohistochemistry and Western blot, separately. RESULTS: ①Compared with the normal group, the average escape latency of Morris water maze test was prolonged in the model group(P<0.05, P<0.01), duration of swimming in the original platform quadrant and the number of original platform crossing were significantly shorter and less respectively (P<0.01). Compared with the model group, the average escape latency in the EA group was shortened (P<0.05, P <0.01), the duration of swimming in the original platform quadrant and the number of original platform crossing were significantly prolonged and increased (P<0.01); The average escape latency in the MA group was shortened (P<0.05, P <0.01),and the duration of swimming in the original platform quadrant was prolonged (P<0.05). Compared with the EA group, the average escape latency of the MA group was prolonged (P<0.05), the duration of swimming in the original platform quadrant was shortened(P<0.05). ②Transmission electron microscopy revealed that the neurons in the hippocampal CA1 area had irregular shape and vague structure, reduction in size and number of mitochondria accompanied with swelling, and malformed changes of mitochondrial crest in the model group, which was relatively milder in both EA and MA groups. ③The expression levels of hippocampal Tau-5, p25 and CDK5 proteins were significantly up-regulated in the model group in contrast to the normal group (P<0.01, P<0.05), and obviously down-regulated in both EA and MA groups relevant to the model group (P<0.05, P<0.01). Compared with the EA group, the expression levels of p25 and CDK5 proteins were significantly increased in the MA group (P<0.05). CONCLUSION: EA of BL23 can improve the learning-memory ability in SAMP8 mice, which is associated with its effect in down-regulating the expression of hippocampal CDK5, p25 and Tau-5 proteins.

14.
Acupuncture Research ; (6): 281-286, 2020.
Article in Chinese | WPRIM | ID: wpr-844164

ABSTRACT

OBJECTIVE: To investigate the effect of electroacupuncture (EA) combined with Donepezil on learning-memory ability and gene expression of β-amyloid (Aβ) clearance-related factors in the hippocampus in senescence-accelerated mouse prone 8 (SAMP8) mice, so as to explore their synthetic effect in improving dementia of Alzheimer's disease (AD).. METHODS: Male SAMP8 mice (30-week-old) were randomly divided into model, medication and EA+medication groups (n=6 mice in each group), and other 6 senescence-resistant 1 (SAMR1) mice were used as the control group. Mice of the medication and EA+medication group received gavage of Donepezil (1.3 mg•kg-1•d-1) once daily for 4 weeks. EA (2 Hz, 1 mA) was applied to "Baihui"(GV20) and "Yintang" (EX-HN3) for 15 min, once daily, 6 days a week for 4 weeks for rats in the EA+medication group. The Morris water maze (MWM) task (including place navigation tests and space exploration trials) was used to assess the mouse's learning-memory ability. Histopathological changes of hippocampus tissue were observed by H.E. staining. The expression levels of matrix metalloprotein 9 (MMP-9), low density lipoprotein receptor-related protein-1 (LRP-1), P-glycoprotein (Pgp, an important drug transporter responsible for multidrug resistance), Claudin-5 (a component of tight junction strands that serves as a physical barrier to prevent solutes and water from passing freely through the paracellular space between epithelial or endothelial cell sheets of blood-brain barrier, BBB) and Aβ mRNAs of the hippocampus tissue were detected by quantitative real-time PCR. RESULTS: Compared with the control group, the average escape latency of place navigation tests, and the expression levels of MMP-9 and Aβ mRNAs were significantly increased (P<0.01), and the number of platform quadrant-crossing times of space exploration trials, and the expression levels of LRP-1, Pgp and Claudin-5 mRNAs considerably decreased in the model group (P<0.01). After the intervention, the learning-memory ability was significantly improved in the medication and EA+medication groups (P<0.01,P<0.05), the expression levels of Aβ mRNAs in the medication and EA+medication groups and MMP-9 mRNA in the EA+medication group were obviously down-regulated (P<0.01), and those of LRP-1 and Pgp mRNAs in the medication and EA+medication groups and Claudin-5 mRNA in the EA+medication group were remarkably up-regulated (P<0.05, P<0.01). The therapeutic effect of EA+medication was apparently superior to that of simple medication in shortening the escape latency (P<0.05,P<0.01) and in down-regulating the expression of MMP-9 and Aβ mRNAs(P<0.01), and in increasing the number of platform quadrant-crossing times(P<0.01), and expression levels of LRP-1, Pgp and Claudin-5 mRNAs (P<0.01). H.E. staining showed scatted and loose arrangement of neurons in the hippocampus, with reduction of number of cell layers and unclear nucleoli, which was relatively milder in the medication and EA+medication groups. CONCLUSION: EA can enhance the effect of Donepezil in improving learning-memory ability in AD mice possibly by regulating expression of MMP-9, LRP-1, Pgp and Claudin-5 mRNAs and strengthening the effect of Donepezil in transporting Aβ via BBB.

15.
Acupuncture Research ; (6): 275-280, 2020.
Article in Chinese | WPRIM | ID: wpr-844169

ABSTRACT

OBJECTIVE: To investigate the effect of acupuncture stimulation of head acupoints "Jin San Zhen" (JIN's Three Acupuncture Needles Therapy) on behavior reactions, hippocampal neuronal autophagy and expression of autophagy associated proteins (Beclin-1 and light chain 3 Ⅱ/Ⅰ [LC 3 Ⅱ/Ⅰ]) in rats with hypoxic-ischemic brain damage (HIBD) due to fetal intrauterine distress, so as to reveal its underlying mechanisms in improving neonatal HIBD. METHODS: Pregnant SD rats were used in the present study. The HIBD model was established by delayed caesarean delivery and bilateral uterine arteries clipping for 10 minutes. The HIBD rats were randomly divided into model group and acupuncture groups (n=9 rats in each group). The other 9 rats delivered naturally were used as the normal control group. On day 14 after delivery, the neonatal rats in the acupuncture group received acupuncture stimulation of head acupoints ("Nao San Zhen""Nie San Zhen" and "Zhi San Zhen") by twirling each needle leftward and rightward for 10 times, once a day for 14 d. The open field test and Morris water maze test were used to determine the locomotive activity and spatial learning-memory ability, respectively. The ultrastructure and autophagosomes in the hippocampal neurons were observed by transmission electron microscope. The contents and expression levels of Beclin-1 and LC3 Ⅱ/Ⅰ in the hippocampus tissues were detected by flow cytometry and Western blot, separately. RESULTS: Compared with the normal control group, the time to go out of the central region of open field test, and the escape latency and duration of first platform-quadrant-crossing of spatial exploration of Morris water maze tests were significantly increased (P<0.01,P<0.05,P<0.001), and the total distance and number of activities in the central region, and the target quadrant resistance time and number of platform-cros-sing remarkably decreased in the model group (P<0.01, P<0.05), suggesting a decline of both locomotor activity and learning-memory ability after modeling. The expression level (%) of Beclin-1 protein and ratio of LC3 Ⅱ/Ⅰ proteins were considerably increased in the model group (P<0.01). Following acupuncture interventions, the locomotor activity and spatial learning-memory ability were obviously increased (P<0.05,P<0.01,P<0.001), and the expression of Beclin-1 protein and ratio of LC3 Ⅱ/Ⅰ were further up-regulated relevant to the model group (P<0.001). Moreover, ultrastructural observation showed serrated change of nuclear membrane and widened perinuclear space, vacuolization in the mitochondria, dilation of endoplasmic reticulum and increase of autophagosomes in the hippocampal neurons in the model group. These situations were relatively milder in the acupuncture group. CONCLUSION: Acupuncture of head acupoints of "JIN San Zhen" may increase locomotor activity and learning-memory abi-lity in rats with HIBD due to fetal intrauterine anoxia, which is closely with its effect in promoting hippocampal neuronal autophagy via up-regulating the expression of Beclin-1 and LC3 Ⅱ/Ⅰ.

16.
Acupuncture Research ; (6): 21-26, 2020.
Article in Chinese | WPRIM | ID: wpr-844211

ABSTRACT

OBJECTIVE: To observe the effect of electroacupuncture (EA) stimulation on the expression of c-Jun terminal kinase(JNK)signaling pathway-related proteins in the hippocampus of vascular dementia (VD) rats, so as to explore its mechanisms underlying improvement of VD. METHODS: Male Sprague-Dawley rats were randomly divided into sham operation, model and EA groups (n=10 rats per group). The VD model was prepared by repeated occlusion of the bilateral common carotid arteries for 10 min and reperfusion for 10 min (3 times in total). The rats in the EA group received EA (2 Hz, 2 mA) at "Dazhui"(GV14),"Baihui"(GV20), and bilateral "Housanli"(ST36) ,"Geshu"(BL17) for 10 min, once daily for 14 days. The learning-memory abi-lity was detected by Morris water maze tests, the distribution of hippocampal neurons detected by Nissl staining, and the apoptosis of hippocampal neurons detected by using TdT-mediated dUTP nick-end labeling (TUNEL) method. The expressions of JNK, phosphorylated JNK (p-JNK), cysteine-containing aspartate-specific proteases-8 (Caspase-8) and Caspase-3 proteins were detected by Western blot. RESULTS: After modeling and compared with the sham operation group, the escape latency was significantly prolonged (P<0.01) and the number of safe-platform quadrant crossing obviously decreased (P<0.01), suggesting a reduction of learning-memory ability. The number of hippocampal neurons was considerably reduced (P<0.01), and that of hippocampal apoptotic neurons remarkably increased in the model group (P<0.01). Whereas, the expression levels of hippocampal apoptosis-related proteins as JNK, p-JNK, Caspase-8 and Caspase-3, as well as the apoptotic index were significantly up-regulated (P<0.01). Following EA intervention, the learning-memory ability was apparently improved (P<0.01), and the number of hippocampal neurons was considerably increased (P<0.01), the hippocampal apoptotic cell number, apoptosis index and the expression levels of JNK, p-JNK, Caspase-8 and Caspase-3 were significantly down-regulated (P<0.01). CONCLUSION: EA intervention can improve the learning-memory ability of VD rats, which may be associated with its effects in reducing hippocampal apoptosis by suppressing JNK signaling pathway.

17.
Chinese Journal of Neuromedicine ; (12): 787-793, 2020.
Article in Chinese | WPRIM | ID: wpr-1035281

ABSTRACT

Objective:To investigate whether astragaloside (AST) IV can improve spatial learning and memory abilities by alleviating oxidative stress damage to the frontal cortex and hippocampus in vascular dementia (VD) rats induced by chronic cerebral ischemia.Methods:Totally, 72 adult male Wistar rats were randomly assigned to four groups: sham-operated group ( n=12), model group ( n=20), AST-IV 10 mg group ( n=20), and AST-IV 20 mg group ( n=20); chronic cerebral ischemia-induced VD models in the later three groups were established by permanent bilateral common carotid artery occlusion (BCCAO); 3 h after BCCAO, these rats were administered with saline, 10 mg/kg AST-IV, or 20 mg/kg AST-IV once daily for a consecutive 90 d. Ninety-four d after modeling, spatial learning and memory abilities were assessed by Morris water maze; the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT), and malondialdehyde (MDA) levels were measured by enzyme linked immunosorbent assay (ELISA). The levels of lipid peroxidation and oxidative DNA damage were assessed by immunohistochemical staining for 4-hydroxynonenal (4-HNE) and 8-hydroxy20-deoxyguanosine (8-OhdG), respectively. Results:(1) On the 3 rd, 4 th and 5 th d of place navigation test, the escape latency in rats of the model group was significantly longer than that in the sham-operated group, and that in the AST-IV 20 mg group was significantly shorter than that in the model group ( P<0.05); spatial probe test showed that the time percentage of rats spending in platform region in the model group (20.3%±1.7%) was significantly smaller than that in the sham-oprated group (48.2%±3.6%), and that in the AST-IV 20 mg group (39.7%±3.2%) was significantly larger than that in the model group ( P<0.05). (2) As compared with those in the sham-operated group, the SOD, GSH-Px and CAT activities were statistically decreased while MDA level was significantly increased in the frontal cortex and hippocampal CA1 area of rats in the model group ( P<0.05); as compared with those in the model group, the SOD, GSH-Px and CAT activities were statistically increased while MDA level was significantly decreased in the frontal cortex and hippocampal CA1 area of rats in the AST-IV 20 mg group ( P<0.05). (3) As compared with those in the model group, the numbers of 4-HNE and 8-oHdG positive cells in the frontal cortex and hippocampal CA1 area of rats in the AST-IV 20 mg group were significantly smaller ( P<0.05). Conclusion:Intraperitoneal injection of high dose AST-IV can ameliorate oxidative damage in the frontal cortex and hippocampal CA1 area in chronic cerebral ischemia-induced VD models, and has the potential to reverse spatial learning damages and memory dysfunction.

18.
Zhongguo zhenjiu ; (12): 68-74, 2020.
Article in Chinese | WPRIM | ID: wpr-781767

ABSTRACT

OBJECTIVE@#To explore the effect of early intervention electroacupuncture (EA) at "Baihui" (GV 20), "Dazhui" (GV 14) and "Shenshu" (BL 23) on the learning-memory ability and the expression of phosphorylated Tau protein in the hippocampus of SAMP8 mice, so as to provide reference for the intervening period of EA for Alzheimer's disease (AD).@*METHODS@#A total of 36 3-month old SAMP8 mice were randomly divided into a model group, a 3-month-old EA group and a 9-month-old EA group, 12 mice in each group. Twelve normal SAMR1 mice with the same age were taken as the control group. The mice in the 3-month-old EA group and 9-month-old EA group were treated with EA at "Baihui" (GV 20), "Dazhui" (GV 14) and "Shenshu" (BL 23) separately 3 months old and 9 months old (continuous wave, 2 Hz, 1.5-2 mA), 20 min each time, once a day, 8 days as a course of treatment, with an interval of 2 days between courses, totally 3 courses of treatment were given. The mice sample in each group was collected at the age of 10 months after the learning-memory ability tested by Morris water maze. The expression of phosphorylated Tau protein in the hippocampus was detected by immunohistochemistry and Western blot, and the expression of Tau mRNA was detected by real-time PCR.@*RESULTS@#Compared with the control group, in the model group, the escape latency was significantly increased (<0.01), the time of stay in the original platform quadrant and the number of crossing the platform quadrant were reduced (<0.01), and the expressions of phosphorylated Tau protein and Tau mRNA in hippocampus were increased (<0.01). Compared with the model group, in the 3-month-old EA group and 9-month-old EA group, the escape latency was significantly reduced (<0.05), the time of stay in the original platform quadrant and the number of crossing the platform quadrant were increased (<0.05), and the expressions of phosphorylated Tau protein and Tau mRNA in hippocampus were reduced (<0.05). Compared with the 9-month-old EA group, in the 3-month-old EA group, the escape latency was significantly reduced (<0.05), the time of stay in the original platform quadrant and the number of crossing the platform quadrant were increased (<0.05), and the expressions of phosphorylated Tau protein and Tau mRNA were reduced (<0.01).@*CONCLUSION@#The early EA intervention could more effectively improve the learning-memory ability and inhibit phosphorylation of Tau protein in the hippocampus of SAMP8 mice.


Subject(s)
Animals , Mice , Disease Models, Animal , Electroacupuncture , Hippocampus , Learning , Memory , tau Proteins
19.
Zhongguo zhenjiu ; (12): 375-378, 2020.
Article in Chinese | WPRIM | ID: wpr-826727

ABSTRACT

OBJECTIVE@#To compare the therapeutic effect of electroacupuncture (EA) combined with donepezil hydrochloride and donepezil hydrochloride alone on improving learning-memory ability in patients with Alzheimer's disease (AD), and to explore its action mechanism.@*METHODS@#Sixty patients of AD were randomly divided into an observation group and a control group, 30 cases in each group. The patients in the observation group were treated with EA at governor vessel (GV) combined with donepezil hydrochloride. EA was applied at Baihui (GV 20) and Fengfu (GV 16) with dilatational wave (10 Hz/50 Hz of frequency, 0.5 to 5.0 mA of intensity), and the needles were kept for 40 min, EA was given once a day; the donepezil hydrochloride tablet was taken orally, 5 mg, once a day, and after 4 weeks the dosage might be increased to 10 mg per day according to the specific situation. All the treatment was given for 8 weeks. The patients in the control group were only treated with donepezil hydrochloride with the identical procedure as the observation group. The Montreal cognitive assessment (MoCA) and Alzheimer's disease assessment scale cognitive part (ADAS-Cog) were evaluated before and after treatment; P300 (latency and amplitude of N2 and P3) was detected by EEG/ERP system brain event related potential instrument, and amyloid precursor protein (APP) and β-amyloid protein 1-42 (Aβ) were detected by ELISA.@*RESULTS@#Compared before treatment, the MoCA scores were increased after treatment in the two groups (<0.05), and the MoCA score in the observation group was higher than that in the control group (<0.05). Compared before treatment, the ADAS-Cog scores were decreased after treatment in the two groups (<0.05), and the ADAS-Cog score in the observation group was lower than that in the control group (<0.05). Compared before treatment, the latency of N2 and P3 was shortened and the amplitude was increased after treatment in the two groups (<0.05); after treatment, the latency of N2 and P3 in the observation group was shorter than that in the control group and the amplitude was higher than that in the control group (<0.05). Compared before treatment, the serum levels of APP and Aβ were lower after treatment in the two groups (<0.05), and the serum levels of APP and Aβ in the observation group were lower than those in the control group (<0.05).@*CONCLUSION@#EA at Baihui (GV 20) and Fengfu (GV 6) combined with donepezil hydrochloride can effectively reduce the serum levels of APP and Aβ and improve the scores of MoCA and ADAS-Cog and the levels of N2 and P3 of P300 in AD patients, which has superior effect to donepezil hydrochloride alone in improving the learning-memory of AD patients.


Subject(s)
Humans , Alzheimer Disease , Blood , Therapeutics , Amyloid beta-Peptides , Blood , Amyloid beta-Protein Precursor , Blood , Cognition , Donepezil , Therapeutic Uses , Electroacupuncture , Learning , Memory , Peptide Fragments , Blood
20.
Article in Chinese | WPRIM | ID: wpr-821083

ABSTRACT

@#To investigate the neuroprotective effect and possible molecular mechanism of PNU-282987 on rats subjected to ischemia and reperfusion. In this study, middle cerebral artery occlusion/reperfusion(MCAO/R)in rats was used as the animal model. The 44 Sprague-Dawley(SD)rats were divided into 4 groups, sham group, model group, low-dose of PNU-282987(1. 2 mg/kg)and high-dose of PNU-282987(2. 4 mg/kg)treatment group. Y-maze test was tested for the learning and memory abilities of rats, and we also examined the brain infarct size, brain edema and neurological dysfunction in rats. Furthermore, HE staining was used to evaluate the neuronal injury and TUNEL assay was used to evaluate the neuronal apoptosis in the rat brain. The results revealed that the learning and memory abilities of rats in treatment group improved significantly, and treatment with PNU-282987 reduced brain infarct size, lessoned brain edema, lessened neurological dysfunction, ameliorated pathological injury and prevented neuronal apoptosis. The above results suggest that the underlying mechanism of PNU-282987 on improving learning and memory abilities of rats after cerebral ischemia and reperfusion may include the inhibition of neuronal apoptosis.

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