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The post-stroke depression (PSD) is one of the common complications of stroke.It can not only delay the recovery of the neurological function in patients, seriously affect the quality of life of patients, but also increase the mortality and morbidity.More and more attention has been paid to the pathogenesis of PSD.Recent studies have confirmed that brain small vessel disease is closely related to the occurrence of PSD.This article reviews relationship between brain small vessel diseases and PSD.
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Objective To investigate the effects of peroxisome proliferators-activated receptorγ(PPARγ)agonist pioglitazone on the expressions of glial fibrillary acidic protein (GFAP) and cyclin D1 in the hippocampal CA1 region after cerebral ischemia in rats.Methods Fifty-four Sprague-Dawley rats were randomly divided into 3 groups:sham operation group,ischemia/reperfusion group,and pioglitazone intervention group (18 in each group).A rat middle cerebral artery occlusion and reperfusion model was induced by the modified suture method.Continuous pioglitazone rosiglitazone gavage (0.65 mg/kg once a day) was conducted for 5 days before modeling in the pioglitazone intervention group.At day 1,3,and 7 after modeling the rats (6 at each time point) were sacrificed and their brains were removed.HE staining was used to detecte the pathological changes of neurons in the hippocampal CA1 region.Immunohistochemical staining was use to detect the expressions of GFAP and cyclin D1 in the hippocampal CA1 region.Results Compared to the sham operation group,at day 3 and 7 after ischemia/reperfusion,the number of neuronal survival in the hippocarmpal CA1 region in the ischemia/reperfusion group was significantly reduced (all P ＜ 0.01).The expressions of GFAP and Cyclin D1 at all time points were significantly upregulated (all P ＜ 0.01).At day 3 and 7 after ischemia/reperfusion,the numbers of neuronal survival in the hippocampal CA1 region in the pioglitazone intervention group were significantly increased (all P ＜0.01).Compared to the ischemia/reperfusion group,the expressions of GFAP and Cyclin D1 at all time points were significantly down-regulated (all P ＜ 0.01).Conclusions PPARγagonist pioglitazone has a significant protective effect on neuron in the hippocampal CA1 region after cerebral ischemia/reperfusion in rats.Its mechanism may be associated with inhibiting GFAP and cyclin D1 expressions.
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Thiazolidinodiones are a synthetic ligand of peroxisome proliferator-activated receptor γ(PPARγ).PPARγhas certain protective effects for several types of tissues.The research covers the areas of glucose,lipid metabolism,cancer and atherosclerosis,etc.At present,the roles of thiazolidinediones in central nervous system diseases have received much attention,such as cerebral infarction,multiple sclerosis,and Alzheimer's disease.This article reviews the effects of PPARγ ligand thiazolidinediones on inhibiting the proliferation of glial cells,promoting angiogenesis,and antagonizing neuronal apoptosis after cerebral ischemia.
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Dyslipidemia refers to the elevated cholesterol,triacylglyceride levels and/or the reduced high density lipoprotein level.It is the important risk factor for the occurrence of atherosclerosis,and it is alsoassociated with the onset and outcome of acute cerebrovascular disease.Therefore,the highly efficient and comprehensive lipid lowering therapy has become one of the most important and effective prevention measures for cerebrovascular disease.This article reviews the recent advances in research on dyslipidemia and lipid lowering therapy in patients with cerebrovascular disease.
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Cerebral vasospasm (CVS) is one of the serious complications of subarachnoid hemorrhage (SAH).Pathogenesis of CVS has not been fully clarified,and it may be associated with a variety of factors.With the development of molecular biology techniques,people have more understanding on SAH caused pathogenesis of CVS,and the research has also made considerable progress in the prevention of CVS.
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Objective To investigate the significance and mechanism of intracerebroventricular injection viper venom nerve growth factor (Vngf) in rat neural plasticity after cerebral ischemia reperfusion injury.Methods Ninety Wistar male rats were randomly assigned into Vngf-25 U group (n = 18), Vngf-50 U group (n = 18), Vngf-100 U group (n = 18), ischemia reperfusion group (n = 18) and sham operated group.The expression of candidate plasticity-related gene 15(cpg-15) Mrna and nuclear factor of kappa B ( NF-Κb ) Mrna in rat brain tissues which were collection at 2,7,14 days after surgery were evaluated by the real time PCR.Results The expression of cpg-15 Mrna and NF-Κb Mrna began to increase after surgery( the F value of cpg-15:70.43, 34.11, 31.89, the F value of NF-Κb: 27.47, 34.56, 31.89,P＜0.01).At the same time, expression of cpg-15 Mrna and NF-Κb Mrna in the Vngf groups was significantly different from the I/R group and the sham operated group (the F value of cpg-15:48.18, 55.93, 78.43, the F value of NF-Κb: 45.92, 55.72, 50.49, P ＜0.01).The more Vngf were injected, the more cpg-15 Mrna and NF-Κb Mrna were expressed in Vngf groups.Conclusions The Vngf could accelerate neural plasticity and restore neurofunctional defect through up-regulated the expression of cpg-15 and NF-Κb.
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S100B is a class of acid calcium-binding protein. It mainly exists in neuroglial cells in the central nervous system, and it is one of the signs of astrocyte activation. S100B may reflect the function of neuroglial cells and regulate the complex interactions between the neurons and neuroglial cells. Studies in recent years have demonstrated that S100B protein is involved in the pathological processes of acute ischemic brain injury. Serum S100B protein can be used as an important marker for identifying the severity of cerebral infarction, progress and outcome.
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Brain ischemic conditioning (BIP) can improve the tolerance to ischemic injury in the brain. Nuclear factor-κB (NF-κB) is an important transcriptional regulatory factor.It presents in all types of cells in the nerous system. Studies have suggested that BIP may exert neuroprotective effects by mediating NF-κB through a series of cascade reactions. This may provide a new therapeutic strategy for BIP in the prevention and treatment of ischemic cerebrovascular disease in clinical practice.
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@#ObjectiveTo explore the Apolipoprotein-E （ApoE） gene polymorphism in patients with Alzheimer's disease （AD）, vascular dementia (VD) or mild cognitive impairment (MCI). MethodsPeripheral blood was taken from patient with AD, VD or MCI to determine the ApoE genotypes. ResultsThe most of the patients were ε3/ε3 genotype, while the ε2/ε2 and ε4/ε4 could not be detected. ε3/ε4 genotype （P=0.001） and ApoE ε4 allele （P=0.013） was more frequent in AD than in MCI. ApoE ε4 was more frequent in VD than in MCI （P=0.044）. ConclusionApoE ε4 allele is a risk factor in AD, and may be associated with VD and MCI.
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Objective To investigate the effects of Ginkgo biloba extract EGb761 on the expressions of XIAP and Smac following focal cerebral ischemia in rats. Methods A total of 40 male Wistar rats were randomized into 4 groups: sham-operation group, cerebral ischemi-a/reperfusion group, low-dose EGb761 group, and high-dose EGb761 group (n=10 in each group). A rat model of middle cerebral artery occlusion (MCAO) for 1.5 hours and reperfusion for 24 hours was built. EGb761 50 mg/kg and 100 mg/kg were injected intraperitoneally at one hour before the model building in the low-dose EGb761 and high-dose EGb761 groups. The expressions of XIAP and Smac in brain tissue were detected by immunohistochemistry method. Results The expressions of XIAP were 18. 33±4. 01 and 26. 7±3.27 respectively in the low-dose EGb761 and high-dose EGb761 groups, and they were significantly higher than 12. 13±3.44 in the cerebral ischemia/reperfusion group (all P<0.01), and the high-dose EGb761group was higher than the low-dose EGb761 group (P<0.01). 1he expressions of Smac in brain tissue were 21.33±3.15 and 11.33±2. 10 respectively in the low-dose EGb761 and high-dose EGb761 groups, and they were significantly lower than 28.93±4. 96 in the cerebral ischemia/reperfusion group (all P<0.05). The high-dose EGb761 group was significantly lower than the low-dose EGb761 group (P<0.05). Conclusions Cerebral ischemia/reperfusion could induce the expressions of XIAP and Smac. EGb761 intervention could inhibit the expressions of Smac while upregulating the expression of XIAP, and increase the XIAP/Smac ratio. 1his may be one of the protective mechanisms of EGb761 intervention.
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@# Objective To investigate the cerebral ischemia/reperfusion protection mechanism of viper venom nerve growth factor(vNGF) by the change of expression of growth associated protein-43 (GAP-43) and neurological function.Methods 45 adult male Wistar rats (weight 220～280 g) were divided randomly into 3 groups: sham group(S, n=9), balanced salt solution group (BSS, n=9) and venom nerve growth factor group (vNGF, n=27). Each group was observed for 7 days. vNGF group was divided into 25 U, 50 U and 100 U subgroups respectively. The following indexes in 3 groups were observed respectively: neurologic deficits and the expression of GAP-43 (immunohistochemistry method).Results Neurological function: The scores of neurological function was 0 in S group. The neurological deficits score was lower at the same time in vNGF group than that in BSS group (P<0.05). Immunohistochemistry: GAP-43 expressed in both BSS group and vNGF group. The expression of GAP-43 in vNGF group increased in 25 U, and to maximum in 100 U. The expression of GAP-43 in BSS group was significantly lower than in vNGF group (P<0.05). Conclusion vNGF can effectively enhance and prolong the expression of GAP-43, increase the survival rats of nerve cells, and has the protection effect on nerve cells after cerebral ischemia injured.
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Nerve growth factor may play its particular role in promoting the development of neuroplasticity after central nervous system and peripheral nerve injury. Its possible mechanisms are associated with regulation of TrkA receptor, activation of L-type calcium channel, promoting the release of acetylcholine, regulation of long-term potentiation and long-term depression. The study of the mechanisms of nerve growth factors for promoting neuroplasicity may provide novel therapeutic approaches for the treatment and rehabilitation of stroke, Alzheimer's disease, and peripheral nerve injury, and it may facilitate the development of the therapeutic drugs.
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@# ObjectiveTo study the effect of topiramate on the expression of Heat Shock Protein 70 (HSP70) after brain ischemia and reperfusion injury.MethodsWistar rats were performed operation of double renal artery stenosis to make hypertension. 2 months after, the rats were separated into 3 groups randomly: topiramate group,ischemic reperfusion group and fake operation control group. The rats were performed operation of middle cerebral artery occlusion (MCAO) and made them in ischemia for 2 h. One day later, their brains were obtained, and the number of positive and negtive cells were counted by computerized pathological image analyzer.ResultsThe HSP70 expression of topiramate group was higher than that of ischemic reperfusion group(P<0.05).No positive cell had been found in the samples of the control group.ConclusionTopiramate can enhance the expression of HSP70 and may therefore protect the ischemic brain tissue from reperfusion injury.