Objective: To investigate the effect of Shenfu Injection (SF, ginesenoside and aconite alkaloid) on the apoptosis of intestinal mucosal epithelial cells during ischemia-reperfusion in rats and its potential mechanisms. Methods: Ischemia-reperfusion model was established in rats. Twenty-four rats were divided into 3 groups with 8 rats in each, eg, ischemia-reperfusion (I/R) group, SF-treated group, and control group. In both SF and I/R groups, the superior mesenteric artery was closed with forceps for 1 hour and then reperfused for 2 hours. Either SF (3 ml/kg, SF group) or normal saline (I/R and control groups) was injected intravenously and continuously for (5 ml/kg) with a micropump before the superior mesenteric artery was closed. The superior mesenteric artery was not closed for animals in control group. The expression of casapse-3 and Fas, and the level of TNF-α and pathological changes of the ileal mucosal tissue were assayed. Results: (1) The number of apoptosis cells increased obviously in I/R group and was significantly higher than that in SF and control groups (P<(0.05)). (2) The expression of caspase-3, Fas, and TNF-α was significantly higher in I/R group than SF and control groups (P<(0.01)); however, there was not significant difference in the expression of capase-3 between control group and SF group. There was a positive correlation between the expression of caspase-3, Fas, and TNF-α, and the number of apoptosis cells. (3) Under light microscope, intestinal mucosal impairment was found milder in SF group than (I/R) group (P<(0.05)). Conclusions: SF can depress the apoptosis of intestinal mucosal epithelial cells during ischemia-reperfusion by restraining the expression of TNF-α, Fas, caspase-3, and accordingly alleviate the ischemia and reperfusion injury of intestinal mucosal epithelial cells. Objective: To investigate the effect of Shenfu Injection (SF, ginesenoside and aconite alkaloid) on the apoptosis of intestinal mucosal epithelial cells during ischemia-reperfusion in rats and its potential mechanisms. Methods: Ischemia-reperfusion model was established in rats. Twenty-four Rats were divided into 3 groups with 8 rats in each, eg, ischemia-reperfusion (I/R) group, SF-treated group, and control group. In both SF and I/R groups, the superior mesenteric artery was closed with forceps For 1 hour and then reperfused for 2 hours. Either SF (3 ml/kg, SF group) or normal saline (I/R and control groups) was yet gaseously and continued for (5 ml/kg) with a micropump before the superior Mesenteric artery was closed. The superior mesenteric artery was not closed for animals in control group. The expression of casapse-3 and Fas, and the level of TNF-α and pathological changes of the ileal mucosal tissue were assayed. Results: (1) The number of apoptosis cells increas Ed obviously in I/R group and was significantly higher than that in SF and control groups (P<(0.05)). (2) The expression of caspase-3, Fas, and TNF-α was significantly higher in I/R group Than SF and control groups (P<(0.01)); however, there was not significant difference in the expression of capase-3 between control group and SF group. There was a positive correlation between the expression of caspase-3, Fas, and TNF-α, and the number of apoptosis cells. (3) Under light microscope, intestinal mucosal impairment was found milder in SF group than (I/R) group (P<(0.05)). Conclusions: SF can depress the apoptosis of Intestinal mucosal epithelial cells during ischemia-reperfusion by restraining the expression of TNF-α, Fas, caspase-3, and wearing back the ischemia and reperfusion injury of intestinal mucosal epithelial cells.