Objective To investigate the vascular protective effect of pretreatment with candesartan on cerebral ischemia in rats.Methods Forty-eight male Sprague Dawley rats were randomly divided into sham operation,ischemia-reperfusion,low-dose candesartan group was randomly redivided into reperfusion 24 h and 72 h subgroups (n = 6).A model of middle cerebral artery occlusion was induced by intraluminal suture method after 4 weeks of drug gavage.Blood pressure was measured preoperatively.The neurological scores were performed after 24 and 72 hours of reperfusion.Then the rats were decapitated and the brains were removed.The infarct volume was measured using 2,3,5-triphenyltetrazolium chloride staining.The expression of vascular endothelial growth factor (VEGF) protein in ischemic regions was detected by immunohistochemical staining and Western blot analysis.Results The neurological scores of the low-dose and high-dose candesartan groups at 24 and 72 hours after reperfusion were significantly better than those of the ischemia-reperfusion group (P = 0.008and 0.001,respectively),and the infarct volume was reduced significantly (P=0.010 and 0.000,respectively).At the second week after medication,the blood pressure was decreased significantly in the high-dose candesartan group,and there was no significant antihypertensive effect in the low-dose candesartan group.The positive expression of VEGF mainly distributed in the vascular endothelial cells around the infarcts.Its expression was further upregulated with the time.It reached the peak after 72-hour reperfusion.The result of Western blot analysis was consistent with that of immunohistochemical staining.Conclusions Candesartan may reduce the infarct volume by upregulating the expression of VEGF in the ischemic region and improve the neurological score.

AIM To study the protective effect of curcumin (Cur) on PC12 cells damage induced by oxidative stress. METHODS Using H 2O 2-induced PC12 cells damage as the model of neuron damage induced by oxidative stress, the proliferation of PC12 cells was observed by 3-[4,5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide(MTT)assay, the apoptosis of PC12 cells was detected by propidium iodide stain flow cytometry (FCM), the mitochondrial membrane potential (△?m) was analyzed by rhodamine123 stain FCM and the level of reactive oxygen species (ROS) in PC12 cells was analyzed by dihydrohodamine123 stain FCM. RESULTS In the presence of Cur (20 and 40 ?mol?L -1), the inhibitory rates of PC12 cells induced by H 2O 2 from 25 to 400 ?mol?L -1 and the apoptosis of PC12 cell induced by 100 and 200 ?mol?L -1 H 2O 2 for 24 h were decreased. The level of △?m was decreased significantly in PC12 cells after 100 and 200 ?mol?L -1 H 2O 2 treatment for 24 h, however, those decreases were significantly ameliorated by Cur (20 and 40 ?mol?L -1) treatment. The level of ROS was significantly increased in PC12 cells exposed to H 2O 2 (100 and 200 ?mol?L -1) for 12 h, whereas 40 ?mol?L -1 of Cur prevented the rise induced by H 2O 2. CONCLUSIONS Cur has protective effect on PC12 cells damage induced by oxidative stress and the effect might be attributed to its removal of ROS and increase of △?m level.

ObjectiveTo explore the effects of the serum of traditional Chinese medicine Nao Yi An on glutamate induced cell death in cultured hippocampal neurons of rat and the underlying mechanisms. MethodsHippocampal neurons were cultured. The excitatory amino acid induced toxicity on cultured neurons was investigated. The viability of injured neurons was determined with the measurement of Lactate dehydrogenase (LDH) activity. Mitogen activated protein kinase (MAPK) were determined by immunoprecipitation /kinase assays /western blot detection.ResultsThe serum of Nao Yi-An raised cell viability. The serum of Nao Yi-An upregulated the expression of extracellular regulated protein kinases(ERK) and downregulated the expression of c-Jun N terminal kinase/stress activited protein kinase(JNK) in cultured neurons. The serum of Nao Yi-An induced upregulation of ERK and its anti death action were prevented with the specific ERKs inhibitor PD98059. Conclusions Activation of ERK signaling together with inhibition of JNK signaling by Chinese medicine Nao Yi-An appears to be an important mechanism for its survival effects on cultured hippocampal neurons.

Objective To investigate the adjustment of miRNA-155 on CD4+ CD25+ Treg regulative T cell in peripheral blood in patients with acute cerebral infarction (ACI) and its pathogenesis. Methods Sixty patients with ACI were divided into three groups according to clinical neurological deficit score. Twenty healthy volunteers were enrolled into the control group. The expression levels of plasma miR-155 mRNA and Foxp3 mRNA were detected by real-time quantitative PCR(qRT-PCR). IL-10 levels in plasma were detected by ELISA. Results Expression of miR-155, Treg, Foxp3 mRNA and levels of IL-10 were significantly increased in patients with ACI compared with normal control group, with statistical differences; Expression of miR-155, Treg, Foxp3 mRNA and levels of IL-10 were gradually increased. The values showed significant statistical difference among the mild, moderate and severe ACI groups (P < 0.01). Among the patients,the levels of miR-155, Treg, Foxp3 mRNA and levels of IL-10 in the survival group were obviously lower than those in the non (P<0.05 or P<0.01). There was a positive correlation between miR-155 and Treg, Foxp3 mRNA (P < 0.01). Conclusion This study suggests that miR-155 is involved in the cell proliferation regulation of CD4+ CD25+ Treg cells,and plays some role in the immunological dissonance with ACI.