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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 bone marrow mesenchymal stromal cells (BMSCs) transplantation after mannitol pretreatment on behavioral performance and synaptophysin expression in the CA3 region in hippocampus of vascular dementia (VD) rats.Methods The BMSCs of rats were isolated and purified by the whole bone marrow adherence method.The rats were subjected for permanent ligation of bilateral common carotid arteries at an interval of 3 days for each carotid artery.At the same time,Sham group was set in parallel.Four weeks after modeling,the VD rats were divided randomly into five groups:(1) VD control group; (2) culture media group; (3) mannitol group; (4) BMSCs group;(5) mannitol with BMSCs group.Morris water maze performance and synaptophysin expression in the CA3 region in hippocampus were observed at 4 weeks after transplantation.Results The morris water maze performance significantly improved in mannitol with BMSCs group when compared with BMSCs group,VD control group,culture media group,mannitol group.Moreover,the escape latency of fifth day decreased significantly ((9.3 ±2.9),(14.1 ±3.5),(23.5 ±4.4),(22.8 ±4.4),(23.2 ±2.8) s,F =43.900,P =0.000)),and the platform quadrant residence time increased significantly ((40.8 ± 6.3),(34.9 ±5.8),(26.4±4.8),(27.4 ±7.0),(28.5 ±6.2) s,F=13.000,P=0.000)).The synaptophysin expressions of the hippocampal CA3 region were significantly increased in the mannitol with BMSCs group (39 624 ± 7798) when compared with BMSCs group,VD control group,culture media group,mannitol group (27060 ±4668,18 294 ±6446,19 956 ±4244,18 946 ±4953,F =39.206,P =0.000).Conclusions Intravenous BMSCs transplantation after mannitol pretreatment improves the behavioral performance of VD rats and facilitates the synaptophysin expression of hippocampal CA3 region in VD rats than BMSCs transplantation alone.Mannitol pretreatment can amplify the therapeutic effect of intravenous BMSCs transplantation in VD rats.
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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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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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@#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 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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@# 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.