虎杖苷对幽门螺旋杆菌脂多糖诱导的胃黏膜损伤大鼠胃黏膜细胞凋亡及TNF-α水平影响

Effects of polydatin on apoptosis and TNF-α level of gastric mucosa in rats with helicobacter pylori lipopolysaccharide induced gastric mucosal injury

目的研究虎杖苷对幽门螺旋杆菌脂多糖诱导的胃黏膜损伤大鼠胃黏膜细胞凋亡及肿瘤坏死因子-α(tumor necrosis factor,TNF-α)水平影响。方法用脂多糖灌胃构建胃黏膜损伤大鼠模型,给予虎杖苷灌胃处理,对各组大鼠对胃黏膜损伤指数进行评分。取各组大鼠胃黏膜组织,用ELISA法测定TNF-α、白细胞介素-8(interleukin-8,IL-8)水平,用硫代巴比妥酸法测定丙二醛(malonaldehyde,MDA)含量,用黄嘌呤氧化酶法测定超氧化物歧化酶(supev oxide dismutase,SOD)含量,TUNEL测定细胞凋亡,Western blot法测定剪切的含半胱氨酸的天冬氨酸蛋白水解酶3(Cleaved Caspase-3)、剪切的含半胱氨酸的天冬氨酸蛋白水解酶9(Cleaved Caspase-9)蛋白水平。结果脂多糖灌胃处理后的大鼠胃黏膜损伤指数增加,TNF-α、IL-8水平升高,SOD水平下降,MDA水平也升高,细胞凋亡率升高,Cleaved Caspase-3、Cleaved Caspase-9蛋白水平升高,与未用脂多糖处理的大鼠相比,差异具有统计学意义(P<0.05)。虎杖苷处理后的胃黏膜损伤大鼠的胃黏膜损伤指数降低,TNF-α、IL-8水平降低,SOD水平升高,MDA水平下降,细胞凋亡率降低,Cleaved Caspase-3、Cleaved Caspase-9蛋白水平降低,与胃黏膜损伤大鼠模型相比,差异具有统计学意义(P<0.05)。结论虎杖苷可以减少幽门螺旋杆菌脂多糖诱导的胃黏膜损伤大鼠胃黏膜细胞凋亡,减少炎症因子合成,降低氧化损伤。

Objective To study the effects of polydatin on apoptosis and TNF-α level of gastric mucosa in rats with helicobacter pylori lipopolysaccharide induced gastric mucosal injury. Methods The rat model of gastric mucosal injury was established by lipopolysaccharide, and the rat model of gastric mucosa injury was constructed. Polydatin was given by gavage. The index of gastric mucosal injury was evaluated in each group, and gastric mucosa tissue of rats in each group was taken. The level of TNF-α and IL-8 was measured by ELISA method, and the content of MDA was determined by thiobarbituric acid method. The content of SOD was determined by xanthine oxidase method, and TUNEL assay cell apoptosis, the level of Cleaved Caspase-3 and Cleaved Caspase-9 protein was measured by Western blot method. Results The gastric mucosal injury index of rats increased after lipopolysaccharide gavage, and the level of TNF-α and IL-8 increased. SOD level dropped, and the level of MDA was also increased. The rate of apoptosis was increased, and the levels of Cleaved Caspase-3 and Cleaved Caspase-9 protein were elevated. Compared with the rats that were not treated with lipopolysaccharide, the difference was statistically significant （ P 〈0.05）. The gastric mucosal damage index of rats with gastric mucosal injury after polydatin treatment was reduced, and the level of TNF-α and IL-8 was reduced. The level of SOD was elevated. MDA level dropped. The rate of apoptosis was reduced, and the levels of Cleaved Caspase-3 and Cleaved Caspase-9 protein were decreased. Compared with the rat model of gastric mucosal injury, the difference was statistically significant （ P 〈0.05）. Conclusion Polydatin can reduce the apoptosis, the synthesis of inflammatory factors, and reduce oxidative damage of gastric mucosa cells induced by lipopolysaccharide in helicobacter pylori.