Objective To study the relationship between ischemic stroke and gene polymorphism of an-giotensin-converting enzyme (ACE), apolipoprotein E (APOE) and methylene tetrahydrofolate reductase (MTHFR) among the population of Zhuang nationality in western Gui. Methods We directly sequenced ACE, APOE and MTHFR genes in 149 cases of ischemic stroke and 109 cases of normal people in western Gui. χ2 test was used to measure the relationship between gene polymorphism and ischemic stroke. Hardy-Weinberg genetic equilibrium test was used to evaluate the reliability of these data. Results In the ischemic stroke group, 62 cases, 22 cases and 65 cases carried II genetype, DD genetype and ID genetype in ACE. χ2 test showed no relationship between ACE gene polymorphism and ischemic stroke. In analysis of the polymorpism of APOE in the ischemic stroke and control group, no relationship between APOE gene polymorphism and ischemic stroke was found by χ2 test. MTFHR gene polymorphism was significantly related with ischemic stroke by χ2 test (P = 0.019). Conclusion Polymorphism of gene MTFHR but neither ACE nor APOE is significantly associated with ischemic stroke.

Omega-3 polyunsaturated fatty acids are a kind of nutrients mainly derived from deep-sea fish, and their role in cardiocerebrovascular diseases has been extensively studied. This article reviews the correlation between omega-3 polyunsaturated fatty acids and the risk and outcome of ischemic stroke and its mechanism of action.

AIM:To investigate the impact of aquaporin 4(AQP4)expression inhibition on autophagy and apoptosis in a mouse model of cerebral ischemia-reperfusion(I/R)injury,and to elucidate its underlying mechanism.METHODS:Cerebral I/R injury was induced in mice via transient middle cerebral artery occlusion(tMCAO).Totally 60 mice were randomly divided into sham group,I/R group,AQP4 inhibition group,and 3-methyladenine(3-MA)group,with 15 mice in each group.Among them,the mice in sham and I/R groups received intraperitoneal injections of normal saline,while those in AQP4 inhibition group and 3-MA group received intraperitoneal injections of AER-271(2 mg·kg-1·d-1)and AER-271+3-MA(2 mg·kg-1·d-1)for 3 d,respectively,once per day.Longa score was adopted to assess the neu-rological function,and to record changes in body weight.Cerebral infarction volume and histopathological alterations were evaluated using hematoxylin-eosin staining.Western blot analysis was performed to determine the levels of AQP4,LC3-Ⅱ,P62 and cleaved caspase-3,while the LC3-Ⅱ,P62,cleaved caspase-3 and NeuN(neuronal marker)colocalization and expression assessment were conducted with immunofluorescence.RESULTS:The mice in I/R and AQP4 inhibition groups exhibited extensive cerebral infarction,cerebral edema,and elevated Longa scores.However,in comparision to I/R group,the mice in AQP4 inhibition group showed significantly reduced cerebral infarct volume,cerebral edema vol-ume,and Longa score(P<0.05).Additionally,in contrast to sham group,the mice in I/R group displayed increased ex-pression of AQP4,LC3-Ⅱ and cleaved caspase-3(P<0.01),accompanied by decreased body weight and P62 expression(P<0.05 or P<0.01).Furthermore,compared with I/R group,the mice in both AQP4 inhibition group and 3-MA group demonstrated a decrease in the expression levels of AQP4,LC3-Ⅱ and cleaved caspase-3(P<0.05 or P<0.01),along with increased body weight and P62 expression(P<0.05 or P<0.01).Nonetheless,no significant differences were ob-served between AQP4 inhibition group and 3-MA group regarding Longa score,cerebral infarct volume,body weight,and the expression of AQP4,LC3-Ⅱ,cleaved caspase-3 and P62.CONCLUSION:Inhibition of AQP4 expression signifi-cantly reduces cerebral infarction area and nerve injury severity in tMCAO mice.Moreover,AQP4 expression inhibition decelerates autophagy and apoptosis after cerebral infarction,with the additional autophagy inhibitor showing no notable impact on the protective effect of AQP4 inhibition.