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Aim To investigate the protective effect of Banqiao Codonopsis pilosula (BCP) on cognitive function in rats with Alzheimer's disease(AD) induced by Okadaic acid (OA) and its possible mechanism. Methods SD rats were randomly divided into DMSO group, OA group and BCP low, medium, high treatment group. The rats were gavage administered in groups of one week and two weeks. The water maze training was continued for five days before modeling, and modeling was started 24 hours after the training. The bilateral hippocampus of DMSO group was injected with 10% DMSO 1.5 |xL. OA group and BCP treatment group were injected with OA (0. 392 mmol • L"1) 1.5 (iL. The water maze test was used to observe the spatial learning ability of rats. Western blot was used to observe the activity of PP2A, the phosphoryla-tion of Tau protein and the expression of synaptic protein in hippocampus, and the Nissl's staining to observe the changes of Nissl bodies in hippocampus CA1 and CA3. Results Water maze experiments showed that BCP could improve spatial memory impairment in AD rats. Western blot results showed that BCP in-creased PP2A activity, increased synaptic protein expression, and decreased Tau protein phosphorylation. Nissl's staining suggested an increase in the number of Nissl bodies in BCP treatment group. Conclusions BCP can up-regulate PP2A activity, decrease the phosphorylation level of Tau protein, increase the expression of synaptic proteins, and repair damaged neurons.
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Aim To investigate the effect of astragalo- side Ⅳ on focal cerebral ischemia-reperfusion injury in rats.Methods The focal cerebral ischemia/reper-fusion of rat left middle cerebral artery occlusion ( MCAO) was induced by suture method .Male SD rats were randomly divided into sham operation group , cer-ebral ischemia/reperfusion group , astragaloside IV group and solvent control group .Except for the sham operation group , the others were subjected to ischemia 2h and reperfusion 24h.Then, rats with successful model were chosen for the detection of various indexes . Astragaloside IV group was injected intraperitoneally with astragaloside IV(20 mg· kg -1 ) at the same time as reperfusion , while solvent control group was injected with the same amount of solvent .TTC staining was used to detect the volume of cerebral infarction , and Nissl staining to observe the changes of histomorpholo-gy, and transmission electron microscope (TEM) to ob-serve the ultrastructure of the cells .Results There was no neurological deficit in the sham operation group, and the volume of cerebral infarction was zero . Compared with the sham operation group , there were some increased neurological deficits , nerve cell damage and cerebral infarction volume in other groups ( P <0.05) .Compared with the cerebral ischemia/reperfu-sion group , the nerve function damage could be signifi-cantly improved , the damage of neurons reduced , and the volume of cerebral infarction decreased ( P<0.05 ) in astragaloside IV group , and there was no obvious change in the solvent control group ( P>0.05 ) .Con-clusion Astragaloside IV can reduce the focal ische-mia/reperfusion injury in rats and protect nerve cells from damage.
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Aim To assess the effects of Trillium Tschonoskii Maxim ( TTM) decoction on learning and memory dysfunction in Alzheimer’ s disease ( AD ) model rats which induced by okadaic acid( OA) and its possible mechanism. Methods The SD rats were di-vided into ten groups,namely,d DMSO control group, OA group, TTM high-dose ( 0. 5 g·kg-1·d-1) group,TTM medium-dose ( 1 g·kg-1·d-1) group, TTM lower-dose (2 g·kg-1·d-1) group,and these groups were divided into one week and two weeks of gavage. Treatment groups were gavaged with TTM de-coction twice a day. After 5 days of Morris water maze training,treatment groups and AD model groups were injected with OA (0.392 mmol·L-1,1. 5 μL) in bi-lateral hippocampal of the rats. The DMSO groups were injected with 10% DMSO. The spatial memory reten- tion wereas detected by water maze at 24 h after injec-tion. After the test, we prepared sample for Western blot and Nissl’s staining. The Western blotting test was used to detect the PP2A activity and the phospho-rylation of Tau protein in the hippocampus. Nissl’'s staining was used to observe the changes of the number of Nissl’s bodies in the hippocampal CA1 and CA3 re-gions. Results The Morris water maze test showed that after injection of OA, the latency of TTM groups wereas shorter than that of OA groups. Western blot showed that the high dose TTM could increase the ac-tivity of PP2A and decrease the level of Tau phospho-rylation at PS-Tau396,,PT-Tau404. The Nissl’s stai-ning results showed that the number of Nissl’s bodies in the hippocampal CA1 and CA3 regions of OA groups wereas significantly attenuated compared with that of the number of Nissl's bodies in the hippocampal CA1 and CA3 regions than DMSO groups. The number of Nissl’s bodies in high groups were morewas larger than that of OA group. Conclusion The results show that TTM can improve the learning and memory dysfunction in AD model rats which induced by OA. The mecha- nism wasis probably that TTM can increase PP2A ac-tivity and then down-regulate the level of Tau phospho-rylation and improve neural development.
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Objective To explore the role of microRNA-181b (miR-181b) in cerebral ischemic injury in vivo and its mechanism. Methods Using middle cerebral artery occlusion (MCAO) model to mimic ischemic injury in vivo, the heat shock protein A5(HSPA5) protein level was determined by using Western blotting. The extent of neural cell loss in ischemic cortex after MCAO was assessed by Nissl staining. Neurological score was performed to evaluate the degree of cerebral ischemic injury after MCAO. Results We found that miR-181b antagomir down-regulated miR-181b expression levels in cerebral ischemic cortex of mice after MCA0(P <0.05, n =3). MiR-181 b antagomir improved neurological deficit of mice at 24 hours after transient MCAO (P < 0.05, n =6). HSPA5 protein levels were significantly up-regulated in ischemic cortex of mice after MCAO, and miR-181b antagomir further up-regulated HSPA5 (P < 0.05, n=3). Consequently, miR-181b antagonists attenuated neural cell loss in ischemic cortex after MCAO (P <0.05, n=3). Conclusion MiR-181 b plays an important role in ischemic injury of mice through regulating HSPA5 protein level.
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Aim To investigate the protective mechanism of anisodine hydrobromide against cerebral ischemia-reperfusion injury in rats.Methods In vivo: the cerebral ischemia-reperfusion injury model was established by middle cerebral artery occlusion(MCAO)via suture method in rats;the rats were injected anisodine hydrobromide(1.2,0.6,0.3,0.15 mg·kg-1);the morphological changes were detected by HE staining;the Nissl staining was used to count the number of surviving neurons;the activity of CAT and LDH,the LPO contents in the brain tissue were measured;the expressions of Bax,Bcl-2,caspase-3 and p-Akt in brain tissue were detected by Western blot.In vitro: Western blot assay was used to determine the expression of Bax,Bcl-2,caspase-3 and p-Akt protein expression in the OGD-R model of PC12 cells.The signal pathway of anisodine hydrobromide was identified.Results Anisodine hydrobromide with the dose of 0.15 mg·kg-1 could significantly lessen the morphological changes,and improve the number of surviving neurons;the dose of 0.3 and 0.15 mg·kg-1 could significantly improve the activity of CAT;the dose of 0.3 mg·kg-1 could significantly reduce the contents of LPO in the rat brain tissue;the dose of 1.2 mg·kg-1 could significantly decrease the activity of LDH;the dose of 0.15～1.2 mg·kg-1 could inhibit the expression of Bax,promote the expression of p-Akt in rat brain tissue.All the doses except 0.15 mg·kg-1 could promote the expression of Bcl-2 in rat brain tissue.In vitro,the results showed that anisodine hydrobromide in 25～100 μmol·L-1 could significantly improve the expression of Bcl-2 and the ratio of Bcl-2/Bax,and the dose of 50 μmol·L-1 could significantly improve the ratio of p-Akt/Akt.Conclusion The mechanism of anisodine hydrobromide against cerebral ischemia-reperfusion injury model rats might be related to its anti-oxidative activity and the activation of Akt.
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Aim To observe histopathological changes of hippocampus after acute epilepsy induced by penty-lenetetrazole (PTZ)in rats.Methods Five groups as control group,PTZ-induced 24 hours(h)group,PTZ-induced 72 hours group,PTZ-induced 1 20 hours group and PTZ-induced 1 44 hours group were designed.PTZ (64 mg·kg -1 )was administered with a single intrap-eritoneal injection for generalized tonic-clonic sei-zures in the current experiment.Control and PTZ trea-ted animals were sacrificed after specific time points. Brain was dissected out and then evaluated for neuro-pathological changes using Nissl staining and immuno-histochemical technique.Results In this study PTZ-induced hippocampal neuron status apoptosis occurred at 24 hours and was sustained for 1 44 hours after status epilepticus.Whereas,activated caspase-3 and AIF ap-peared at 24 hours and were sustained for 1 44 hours af-ter status epilepticus.Conclusion The results of this study show that the significant histopathological chan-ges of hippocampus appear in the vicinity of 1 20 hours after intraperitoneal injection of pentylenetetrazole.
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Aim To observe the effects of effective fraction of Epimedium,Astragalus,Radix Puerariae on behavioral and pathological changes in a transgenic mouse model of Alzheimer’s disease.Methods Six-month-old APPswe /PS1 ΔE9 transgenic mice were ran-domly divided into 2 groups:model group and effective fraction group,1 0 mice each group.The mice in the effective fraction group were treated with the effective fraction of Astragalus,Radix Puerariae,Epimedium compound for 8 weeks.The C57BL/6J mice were used as negative control group.After 8 weeks,the learning and memory function were measured by Morris water maze,the pathological changes in brain tissue were ob-served by Modified Bielschowsky staining and Nissl 's staining.Results During place navigation trial,the escape latency in the APPswe /PS1 ΔE9 double transgenic model mice was longer than those of the mice of C57 (P 0.05 ). The Modified Bielschowsky staining shows that the neuron fibers of the cerebral cortex of APPswe /PS1 ΔE9 double transgenic mice were enlarged,swelling,and dense.There were senile plaques and nerve fiber tangles in the cerebral cortex of APPswe /PS1 ΔE9 double transgenic mice.The neuron fibers of mice in the effective fraction group were relieved;there was a small amount of senile plaque.The Nissl’s staining shows that the neurons of the cerebral cortex of APPswe /PS1 ΔE9 mice were edema, the number of cells were decreased.The mice in the effective fraction group were free of the disease.Con-clusion The double transgenic APPswe /PS1 ΔE9 mice of AD can simulate the specific pathogenesis of AD, which may be the efficient experimental animal model. The effective fraction of epimedium,astragalus and ra-dix puerariae may have a neuroprotective effect against AD via improving the learning and memory ability,and reduce the cerebral cortex nerve fiber tangles,senile plaques and neurons edema changes.
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OBJECTIVE: Glutamate is a key excitatory neurotransmitter in the brain, and its excessive release plays a key role in the development of neuronal injury. In order to define the effect of nimodipine on glutamate release, we monitored extracellular glutamate release in real-time in a global ischemia rat model with eleven vessel occlusion. METHODS: Twelve rats were randomly divided into two groups: the ischemia group and the nimodipine treatment group. The changes of extracellular glutamate level were measured using microdialysis amperometric biosensor, in coincident with cerebral blood flow (CBF) and electroencephalogram. Nimodipine (0.025 microg/100 gm/min) was infused into lateral to the CBF probe, during the ischemic period. Also, we performed Nissl staining method to assess the neuroprotective effect of nimodipine. RESULTS: During the ischemic period, the mean maximum change in glutamate concentration was 133.22+/-2.57 microM in the ischemia group and 75.42+/-4.22 microM (p<0.001) in the group treated with nimodipine. The total amount of glutamate released was significantly different (p<0.001) between groups during the ischemic period. The %cell viability in hippocampus was 47.50+/-5.64 (p<0.005) in ischemia group, compared with sham group. But, the %cell viability in nimodipine treatment group was 95.46+/-6.60 in hippocampus (p<0.005). CONCLUSION: From the real-time monitoring and Nissl staining results, we suggest that the nimodipine treatment is responsible for the protection of the neuronal cell death through the suppression of extracellular glutamate release in the 11-VO global ischemia model of rat.
Subject(s)
Animals , Rats , Biosensing Techniques , Brain , Cell Death , Electroencephalography , Glutamic Acid , Glycosaminoglycans , Hippocampus , Ischemia , Microdialysis , Neurons , Neuroprotective Agents , Neurotransmitter Agents , Nimodipine , SalicylamidesABSTRACT
ObjectiveTo investigate the protective effect of testosterone on motor neuron after sciatic nerve injury. MethodsTwelve adult C57 male mice were randomly divided into two groups: the sesame oil control group (n= 6) and the testosterone experimental group (n= 6). Unilateral sciatic nerve cutting severed as the animal model. Following operation, sesame oil or testosterone was administered for the control and experimental animals respectively via subcutaneous injection every other day for two weeks. The number and soma area of the anterior horn motor neurons in the lumbosacral cord of the sciatic nerve injury side were then measured on Nissl stained sections. Results In the testosterone group the motor neurons appeared healthier than that in the sesame control group. The neurons were plumper and showed more processes. Their number and average soma size were significantly larger than that in the sesame control (P<0.01). Conclusion The findings demonstrate that testosterone has a significant protective effect on sciatic nerve motor neurons after nerve injury.
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Fourteen adult and immature rabbits were used for the study of laminar scheme of the gray matter in the spinal cord. The spinal sections were cut transversally or sagitally into 80 ?m, 60 ?m, 15?m, and 2?m-thick sections. The sections were stained with toluidine blue or crecyl fast violet for cell body and with Luxol fast blue for myelin sheath. 2?m-thick sections were only stained with pphenylenediamine. In addition, the spinal sections from 2 cases of the animals were treated histochemically for demonstrating AChE activity. According to the Rexed's principle lamination for the cat, we have found that the cytoarchitectonic organization of the rabbit spinal cord was found to be basically similar to that of the cat except for some differences about the extension and structures of the laminae.
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Objective To study the effect of monochromatic light on the distribution of retinal ganglion cells in chicks. Methods Sixty One-day-old male broilers were reared under four light treatments,red(660nm),green(560nm),blue(480nm) and white(400-760nm) by using LED(light-emitting diodes) as light sources until the 49th day(n=15).Light intensity was 15 lux at the height of birds' heads and scheduled for 23hours of light and 1hour of darkness during the entire experiment.The retinas were stained by Nissl-staining and DiI-labeling.The retinal area,cell size and density in ganglion cell layer were estimated by image analysis. Results The retinal area and RGCs' number in the blue and green light groups were higher than that in the red and white light groups(10.35% and 17.07%,P