黄精多糖对H_(2)O_(2)诱导HT22细胞氧化损伤的保护作用

Protective Effect of Polygonatum Polysaccharides on Oxidative Injury Induced by Hydrogen Peroxide in HT22 Cells

目的:研究黄精多糖在过氧化氢(H_(2)O_(2))损伤后海马神经元HT22细胞的保护作用。方法:建立H_(2)O_(2)诱导HT22细胞氧化损伤模型,黄精多糖干预后,观察黄精多糖对HT22细胞活性的影响及形态变化。水溶性四唑蓝法(WST)测定超氧化物歧化酶(SOD)活性,硫代巴比妥酸法(TBA)测定丙二醛(MDA)含量,比色法测定还原型谷胱甘肽(GSH)含量。蛋白免疫印迹法检测凋亡相关蛋白Bax、Bcl-2及核因子NF-E2相关因子(Nrf2)蛋白表达水平。结果:与H_(2)O_(2)模型组相比,黄精多糖组(100、200、400μg/mL)明显提高细胞活性(P<0.05或P<0.01),减少MDA的产生(P<0.05或P<0.01),增加SOD活力和GSH含量(P<0.05或P<0.01),降低Bax蛋白的表达,增加Bcl-2蛋白的表达。此外,黄精多糖还能够上调细胞中Nrf2的表达。结论:黄精多糖能通过增强细胞内抗氧化活性,提高HT22细胞的存活率,从而保护细胞抗氧化损伤,其作用机制与Nrf2通路有关。

Objective:To study the protective effect of Polygonatum Polysaccharides on hippocampal neurons HT22 cells after injury by hydrogen peroxide(H_(2)O_(2)).Methods:The oxidative damage model of HT22 cells induced by H_(2)O_(2) was established.The effect of Polygonatum Polysaccharides on the activity and morphological changes of HT22 cells were observed.The levels of malondialdehyde(MDA)activity and antioxidant enzyme activities of superoxide dismutase(SOD)and glutathione(GSH)activity were determined by respective kits.Meanwhile,western blot was used to detect the protein expressions of Bax,Bcl-2 and NF-E2-related factor 2(Nrf2).Results:Polygonatum Polysaccharides(100,200,400μg/mL)could enhance the cell vitality(P<0.05 or P<0.01),significantly reduce the cell damage caused by H_(2)O_(2).And it could significantly reduce the production of MDA(P<0.05 or P<0.01),increase the activities of SOD and GSH(P<0.05 or P<0.01).In addition,Western blot results showed that Bcl-2 and Nrf2 protein expressions were up-regulated.Bax protein expression were down-regulated by Polygonatum Polysaccharides.Conclusions:Polygonatum Polysaccharides can enhance the intracellular antioxidant activity to improve the survival rate of HT22 cells,thus protect the cells from oxidative damage.And the mechanism is related to Nrf2 pathway.