中文摘要：

目的观察预先给予半夏泻心汤对束缚水浸应激大鼠胃黏膜上皮细胞B细胞淋巴瘤基因-2（Bcl-2）、Bax m RNA表达、活化的半胱氨酸蛋白酶-3（Caspase-3）表达的影响,探讨半夏泻心汤抗应激性胃黏膜损伤的作用机制。方法 40只雄性SD大鼠随机分为空白组、模型组、中药组（半夏泻心汤组）、西药组（奥美拉唑组）。每组动物相应药物灌胃3 d。大鼠束缚水浸应激（WRS）造模。观察大鼠胃黏膜损伤指数（UI）;RT-PCR法检测各组大鼠胃黏膜中Bcl-2、Bax m RNA表达水平;western-blot法检测胃黏膜活化的Caspase-3表达变化。结果与空白组比较,模型组UI明显升高（P〈0.01）,Bcl-2 m RNA表达显著减弱（P〈0.01）,Bax m RNA、活化的Caspase-3表达明显增强（P〈0.01）;与模型组比较,中药组、西药组UI明显降低（P〈0.01）,胃黏膜中Bcl-2 m RNA表达显著上调（P〈0.01）,活化的Caspase-3表达显著下调（P〈0.01）。结论半夏泻心汤可显著对抗应激性胃黏膜损伤,其抗损伤发生的机制之一可能是通过上调胃黏膜中Bcl-2 m RNA表达,下调活化的凋亡执行因子Caspase-3的表达,从而抑制胃黏膜上皮细胞的过度凋亡,发挥胃黏膜抗应激性损伤的作用。

英文摘要：

Objective To observe pre-administration of Banxiaxiexin decoction on Bcl-2, Bax mRNA and Caspase-3 in gastric epithelial cell of restraint plus water-immersion rats. To investigate the mechanism of the Banxiaxiexin decoction on anti-stress-induced gastric mucosal injury. Methods 40 male SD rats were randomly divided into the blank group, model group, Chinese medicine group （Banxiaxiexin decoction group）, western medicine group （omeprazole group）. The animals in every group were given the corresponding medicine by gavage for 3 days. Model of stress-induced gastric mucosal injury in rats by WRS method,the ulcer index （UI） of gastric mucosa in rats was observed. Using RT-PCR to detect The expression of Bel-2 and Bax mRNA was detected by RT-PCR,and the expression of Caspase-3 was determined by using Western-blott. Results Compared with the blank group, the UI of model group was obviously increased （P〈0.01）, the Bel-2 mRNA expression was significantly decreased （P〈0.01）, Bax mRNA and Caspase-3 expression was significantly increased （P〈0.01）; Compared with the model group, the UI in Chinese medicine group and western medicine group was obviously decreased （P〈0.01）, the Bcl- 2 mRNA expression was up--regulated significantly in gastric mucosa （P〈0.01）, and the expression of activated Caspase-3 was down- regulated significantly （P〈0.01）. Conclusion Banxiaxiexin decoction show an obvious anti-stress-induced gastric mucosal injury effect. One of the mechanisms of its anti-injury is probably by up-regulating the Bcl-2 mRNA expression in gastric mueosa and down-regulating apoptosis factor Caspase-3 activation, thereby inhibiting apoptosis of gastric epithelial ceils.