毛蕊异黄酮苷和芍药苷联用对氧糖剥夺再灌注HT22细胞PI3K/AKT信号通路的影响

目的观察并探讨毛蕊异黄酮苷和芍药苷联用对氧糖剥夺再灌注诱导的HT22细胞氧化应激损伤的作用及其机制。方法建立HT22细胞氧糖剥夺再灌注损伤模型,将HT22细胞分为正常对照组、模型组、给药组、尼莫地平组,应用CCK-8法检测细胞存活率,测定毛蕊异黄酮苷和芍药苷联用对HT22细胞活力的影响,检测细胞中乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)及丙二醛(MDA)含量,并采用Western Blot法检测PI3K、AKT蛋白表达水平。结果与正常对照组相比,氧糖剥夺再灌注处理组的HT22细胞存活率明显降低(P<0.01),LDH活性及MDA的含量升高(P<0.05,P<0.01),SOD活力降低(P<0.01),PI3K、AKT蛋白表达明显下降(均P<0.01);与模型组相比,给药组能明显提高氧糖剥夺再灌注损伤后HT22细胞的存活率(P<0.01),降低LDH、MDA的含量(P<0.05,P<0.05),SOD活力提高(P<0.01),PI3K、AKT蛋白表达升高(均P<0.01)。结论毛蕊异黄酮苷和芍药苷联用对氧糖剥夺再灌注诱导的HT22细胞氧化应激损伤具有明显的保护作用,其作用机制可能通过调节PI3K/AKT信号通路实现。

Effects of Combination of Calycosin-7-glucoside and Paeoniflorin on PI3K/AKT Signaling Pathway in Oxygen-glucose Deprivation and Reperfusion HT22 Cells

Objective Oxygen-glucose deprivation reperfusion model was established to observe the effect of combination of calycosin-7-glycoside and paeoniflorin on oxidative stress injury induced by oxygen glucose deprivation and reperfusion in HT22 cells,and further explore whether the PI3K/AKT signaling pathway is the pathway through which it functions.Methods The cells were divided into control group,model group,drugadministered group,and ni modi pine group.Cell viability measured by CCK-8 was used for determination of the effects of the combination of Calycosin-7-glucoside and paeoniflorin on the viability of HT22 cells.Activities of lactate dehydrogenase(LDH),superoxide dismutase(SOD) and level of malondialdehyde(MDA) in the cells were detected;and expression levels of PI3K and AKT proteins were detected by Western Blot.Results Compared with the control group,the cell survival rate of the oxygen glucose deprivation and reperfusion treatment group was significantly decreased,the LDH activity and MDA content were increased,the SOD activity was decreased,and the expression of PI3K and AKT proteins were significantly decreased.Compared with the model group,the drugadministered group significantly improved the survival rate of cells after oxygen deprivation and reperfusion injury,reduced the activity of LDH and content of MDA,increased the activity of SOD,and increased the expression of PI3K and AKT proteins.Conclusion The combination of Calycosin-7-glucoside and paeoniflorin has obvious protective effect on oxidative stress injury induced by oxygen glucose deprivation and reperfusion in HT22 cells,and its mechanism may be achieved by regulating PI3K/AKT signaling pathway.