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OBJECTIVE：To investigate the protective effects of drug-contained serum of Xiaoxuming decoction （XXM）on astrocyte of oxygen and glucose deprivation model rats ，and to explore its mechanisms. METHODS ：The astrocytes of rats were randomly divided into control group ，model group and XXM low-dose ，middle-dose，high-dose groups. The cells in the control group were not treated ；after 2.5 h of OGD ，model group and XXM low-dose ，middle-dose，high-dose groups were reoxygenated for 0，3，6，12 h in 0（i.e. the model group was not added with drugs ），2.5％，5％，10％ of XXM ，respectively. The content of lactate dehydrogenase （LDH）was detected by colorimetry. The reactive oxygen species （ROS）level was detected by fluorescence probe method ，and the expression of Manganese superoxide dismutase （MnSOD）was determined by immunofluorescence double staining method in control group ，model group and XXM high-dose group after 12 h of reoxygenation following OGD. RESULTS ： The content of LDH in the control group was always kept at a low level ；LDH content in the model group gradually increased from （110.99±17.06）U/L to （436.64±55.29）U/L after 0-12 h of reoxygenation following OGD ，which was significantly higher than that in the control group （P＜0.05）. Compared with model group at the same time point after reoxygenation following OGD ，the contents of LDH in the cells of XXM low-dose ，medium-dose and high-dose groups were decreased to different extents ，and showed a time-and dose-dependent trend. The contents of LDH in XXM groups at 6 and 12 h after reoxygenation following OGD were significantly lower than that of the model group （P＜0.05）. At 12 h after reoxygenation following OGD ，the levels of ROS in model group were significantly higher than control group ， while the level of MnSOD was significantly lower than control group（P＜0.05）. The level of ROS in XXM high-dose group hospital.sh.cn was significantly lower than model group ，while the level of MnSOD was significantly higher than model group （P＜0.05）.. CONCLUSIONS：XXM can protect astrocyte by up-regulating sh.cn levels of MnSOD ，scavenging excessive oxygen free radicals ， to relieve the OGD induced astrocytic injury ，with protective effect.
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Objective To investigate the neuroprotective effect of Dengzhan Shengmai capsule (DZSM) in rat cerebral ischemia-reperfusion injury and to explore the mechanism. Methods Rats were divided into Sham group, MCAO group, DZSM group, carbenoxolone (CBX) group and DZSM + CBX group. Each group was assessed for neurological function , infarct volume and the expression of Caspase-3 48 h after reperfusion. Connexin 43 (Cx43) expression of MCAO group was detected 3, 12, 24, 48 h after reperfusion. Results There were lower neurological deficit scores , infarct volume and the expression of Caspase-3 in DZSM , CBX and DZSM + CBX group 48 h after reperfusion when compared with those in MCAO group (P < 0.05) but Cx43 expression level in each group increased after reperfusion at each time point (P < 0.05). Expression of Cx43 was lower in DZSM, CBX and DZSM + CBX group than that in MCAO group (P < 0.05). Lower expression of Cx43 was also seen in CBX and DZSM + CBX group when compared with that in DZSM group (P < 0.05). Conclusion DZSM capsule can improve neurological function , reduce infarct volume and inhibit the expression of Caspase-3. The mechanism may be related to its inhibition of Cx43 expression.
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Background and purpose:In recent years, many studies have showed that elemene liposome is widely used in the treatment of digestive tract tumors, malignant pleural effusion and ascites. This study combined in vitro and in vivoexperiments to observe the inhibitory effect of elemene liposome on the growth of human gastric cancer and the HGC-27 cell line.Methods:In order to screen the optimum concentration of elemene liposome, machine vision automatic live cell observation analysis system (Cell-IQ) was applied to detect the best inhibitory effect on human gastric cancer cell line HGC-27, and the lfow cytometry was applied to further detect the apoptosis of HGC-27 treated with elemene liposome. The model of human gastric cancer peritoneal metastasis in nude mice was established to investigate the intervention of elemene liposome and cisplatin (DDP) on peritoneal cancer index (PCI). CD31 marker of tumor microvessel density (MVD) and the expression of vascular endothelial growth factor (VEGF) in tumor tissues were investigated to explore the mechanism underlying the inhibitory effect on peritoneal metastasis of HGC-27 cells in nude mice.Results:Cell-IQ analysis showed that the inhibitory effect of elemene liposome on HGC-27 presented in a positive concentration-dependent manner, which could not be further enhanced when the concentration exceeded 100 μg/mL with the best reaction time between 4 and 19 hours. Flow cytometry showed that the early apoptosis rate was 45% in the elemene liposome group and only 0.019% in the control group. The early apoptosis rate was signiifcantly higher in treatment group than that in control group (P0.05).Conclusion:Elemene liposome can inhibit human gastric cancer cells at the optimal concentration of 100 μg/mL with the best reaction time between 4-19 hours. Elemene liposome has a clear preventive effect on peritoneal metastasis of human gastric cancer in nude mice. Induction of apoptosis in gastric cancer cells may be the main mechanism underlying the inhibitory effect of elemene liposome on human gastric cancer cells.
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[ ABSTRACT] AIM:To investigate the effect of triptolide on the inhibition of microglial activation in 1-methyl-4-phenyl pyridinium ( MPP+)-induced hemiparkinson disease rats.METHODS:The rat model of Parkinson disease was es-tablished by intranigral injection of MPP +.The rats were randomly divided into sham group, MPP+group, triptolide group and vehicle group.The survival of dopaminergic neurons was detected by the immunofluorescence of tyrosine hydroxylase ( TH) in the substantia nigra ( SN) .The activation of microglia was determined by immunofluorescence of OX-42 ( micro-glia marker) in the SN.The expression of chemokine receptor CX3CR1 in SN was measured by Western blotting.RE-SULTS:Intranigral injection of MPP+increased the fluorescence intensity of the microglial marker, and promoted DA neu-ron degenerative death.Immunohistological analysis showed that the OX-42 density was decreased (P<0.01) and tyrosine hydroxylase (TH) positive neurons were increased in the triptolide group (P<0.01).The expression of CX3CR1 was lower in triptolide group than that in model group (P<0.05).CONCLUSION:Triptolide may improve PA neurons func-tion in MPP+-induced rats through inhibiting CX3CR1 expression and microglial activation.
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AIM:To investigate the integrative treatment of both coenzyme Q 10 ( CoQ10 ) and minocycline in the rats intranigrally intoxicated with 1-methyl-4-phenylpyridinium ( MPP+) .METHODS:The rat model of Parkinson disease ( PD) was established by intranigral microinjection of MPP +.The degree of microglial activation was measured by immuno-fluorescent density of OX-42 ( a microglia marker ) in the substantia nigra ( SN) .The number of viable dopaminergic neurons was determined by counting the tyrosine hydroxylase ( TH) positive neurons in the SN .The behavioral performances were re-vealed with the number of apomorphine-induced rotations , score of forelimb akinesia and vibrissae-elicited forelimb placing a-symmetry.RESULTS:Pretreatment with CoQ10 or intracerebroventricular (icv) posttreatment with minocycline alone pro-vided partial attenuation against MPP +-induced locomotor defects .Integrative therapy provided enhanced beneficial effects , and resulted in a significant attenuation of locomotor disability than any single therapy (all P<0.01).The results of immu-nohistological analysis showed that the TH positive neurons were maximally protected by integrative therapy compared with minocycline group and CoQ 10 group (P<0.01) .CONCLUSION:The integrative therapy of CoQ 10 combined with minocy-cline may offer additional therapeutic benefit to MPP +-induced hemiparkinson rat model .Such neuroprotective strategy of tar-geting different aspect of the neurodegenerative phenotypes may highlight a new therapeutic strategy for future management of PD.
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To investigate the protective effects of Naoshuantong, a compound traditional Chinese herbal medicine, on the main components of neurovascular unit in rats with cerebral ischemia/reperfusion injury.
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OBJECTIVE: To investigate the potential protective role of Cistanche extracts on 1-methyl-4-phenylpyridinium ion (MPP(+))-induced Parkinson's disease (PD) cellular model, and to find out whether this effect is achieved through the regulation of growth arrest- and DNA damage-induced gene 153 (GADD153). METHODS: MPP(+))-induced cellular injury and the protective effect of Cistanche extracts on the SH-SY5Y cell line viability treated by MPP(+)) were investigated by using methyl thiazolyl tetrazolium (MTT) assay. The mRNA of GADD153 in SH-SY5Y cell line treated by MPP(+)) and Cistanche extracts were evaluated by reverse transcriptase-polymerase chain reaction (RT-PCR). The protein level of GADD153 in SH-SY5Y was assessed by Western blotting. RESULTS: Cistanche extracts (100 mug/ml) increased the cell viability (P<0.01). And the mRNA of GADD153 in the Cistanche extracts pretreatment group was much less than that in the MPP(+)) group (P<0.01). The result of Western blotting showed that GADD153 had a lower level in the Cistanche extracts pretreatment group, compared with MPP(+)) group, especially in the 100 microg/ml group (P<0.01). CONCLUSION: Cistanche extracts pretreatment has a protective effect on the MPP(+))-treated SH-SY5Y cell line, and its down-regulation of GADD153 may contribute to the effect.
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0 05). The forelimb functional tests demonstrated that, the number of food pellets eaten by PD rats with the contralateral side of 6 OHDA lesion (17 71?4 82) was significantly reduced compared with the controls (34 43?3 55)( P
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MMP-9 is one of the family of matrix metalloproteinases, which degrades extracellular matrix. MMP-9 is induced by many inflammatory factors, including IL-1?,IL-8 and TNF-?. Meanwhile, MMP-9 potentiates inflammatory factors by aminoterminal processing. The signal transduction by which inflammatory factors induce MMP-9 is also an important part in recent research. This review will give a summary in all these fields.
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AIM: To explore the effect of brain ischemia injury on cell proliferation and nestin expression in cortex and subependymal zone (SEZ). METHODS: Using a local brain ischemia model(MCAO), BrdU positive cells of cortex and subependymal zone (SEZ), also nestin positive cells, were observed by immunohistochemistry. RESULTS: BrdU and nestin positive cells in SEZ of MCAO rats were obviously increased. In cortex, only nestin positive cells were observed. CONCLUSION: Neural stem cells in SEZ and cortex were activated after brain ischemia, it may be related with neural recovery after brain ischemia injury.
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Objective: To investigate the effect of muscone on infarction volume and neuronal glutamate transporter EAAC1 mRNA expression in rats. Methods: Rats were divided randomly, focal ischemic models of middle cerebral artery occlusion (MCAO) were achieved by inserting nylon surgical thread through the internal carotid artery(ICA) into the anterior cerebral artery(ACA). The rats were sacrificed, the brain was stained by TTC and the area of infarcton was measured. The expression of EAACl mRNA in the hippocampal regions was assessed by RT PCR. Results: Muscone could remarkably reduce tbe infarction volume and expression of EAAC1 mRNA. Conclusion: Muscone plays a significant role in against local cerebral ischemia, the mechanism may be related to reducing EEACl mRNA expression.
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Objective: The experiment was undertaken to explore the blood-brain barrier permeability and the gene expression of matrix metalloproteinase-9 (MMP-9) in ischemic cerebra and the impact of Buyanghuanwu Decoction on them. Methods: The (middle cerebral artery occlusion, MCAO) rat model was used. At 1h, 3h, 24h, 48h, 5d after reperfusion. They were measured. Results: In treatment group, the BBB permeability and the MMP-9 gene expression decreased. Conclusion: Buyanghuanwu Decoction can protect the BBB by inhibiting the MMP-9 gene expression.
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AIM: To investigate the changes of neuronal glutamate transporter (EAAC1) at different ischemic times in the rat hippocampus in early stage. METHODS: Brain microinjection of EAAC1 antisense oligodeoxyneucleotide (EAAC1 antisense) was adopted and focal transient ischemia was produced by the filament method of middle cerebral artery occlusion (MCAO). Western blotting and TTC staining analysis were adopted for observing EAAC1 expression and infarction volume in ischemic region .The expression of EAAC1 mRNA and protein at different ischemic times in the rat ischemic hippocampus was assessed by RT-PCR and Western blotting analysis. RESULTS: Compared with EAAC1 sense group, the volume of brain ischemic infarction [(105.67?8.70) mm~3] was reduced after brain microinjection of EAAC1 antisense. Compared with the sham-operated control, EAAC1 mRNA was significantly higher at 6 h and at (24 h) in the hippocampal regions during ischemia, while protein expression was higher at 24 h only. EAAC1 mRNA and protein expression were unchanged at other ischemic times. CONCLUSION: EAAC1 is associated with ischemic injury and its expression is increased in the hippocampal regions after focal cerebral ischemia.
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Endoplasmic reticulum(ER)stress can be caused by disturbances in the function of the ER with the accumulation of misfolded proteins.The ER response is characterized by unfolded protein response(UPR)causing translational attenuation,induction of ER chaperones and degradation of misfolded proteins.In case of prolonged or aggravated ER stress,cellular signals leading to apoptosis are activated.ER stress has been suggested to be involved in human neurodegenerative diseases,such as Alzheimer's disease,Parkinson's disease,and amyotrophic lateral sclerosis,as well as other disorders.Here we will discuss the neurotoxic effect of ER stress in these three major neurodegenerative diseases,and highlight current knowledge in this field that may reveal novel insight into disease mechanisms and help to design better therapies for these disorders.