参附抑制缺血再灌注大鼠肠上皮细胞凋亡的作用及机制

目的:研究参附注射液对缺血再灌注大鼠黏膜上皮细胞凋亡的影响,并探讨其可能机制。方法:采用大鼠肠缺血再灌注模型,24只大鼠随机分为对照组(C组)、缺血再灌注组(I/R组)和参附治疗组(SF组),SF组于阻断前30min静注SF液每100g体重2ml。再灌注2h检测回肠黏膜上皮细胞Caspase-3、Bcl-2蛋白的表达及TUNNEL细胞凋亡检测,同时观察回肠黏膜组织TNF-α水平及病理形态学改变。结果:①凋亡细胞检测显示:I/R组凋亡细胞显著增多,SF组凋亡细胞数较I/R组显著减少而多于C组(均P<0.05);②Caspase-3、Fas蛋白的表达:Caspase-3和Fas表达均为I/R组显著多于SF组和C组(P<0.01),SF组与C组无明显差异。Caspase-3及Fas表达与凋亡细胞数目呈正相关(Caspase-3:r=0.9149,P<0.01;Fas:r=0.6694,P<0.01);③TNF-α表达:TNF-α的表达在I/R组显著高于C组和SF组(均P<0.01),SF组与C组无明显差异。TNF-α表达与凋亡细胞数目呈正相关(r=0.9133,P<0.01);④SF组小肠黏膜病理损伤程度明显减轻I/R组(P<0.01)。结论:参附注射液通过抑制TNF-α、Fas和Caspase-3表达而抑制缺血再灌注期间肠黏膜上皮细胞的凋亡,从而减轻肠黏膜缺血再灌注损伤。

Effects of Shenfu Injection on the Apoptosis of Intestinal Mucosal Epithelial Cells During Ischemia-Reperfusion in Rats

Objective: To investigate effects of Shenfu(SF) injection on the apoptosis of intestinal mucosal epithelial cells during ischemia-reperfusion in rats and discuss the mechanisms.Methods: Ischemia-reperfusion model was established in rates, twenty-four rats were divided randomly into control group, ischemia-reperfusion group (I/R group) and shenfu injection (SF group). The rat's gut were cut to sections for HE and Tunnel staining, Caspase-3 and Fas protein was assayed by immunohistochemical staining, and the blood sample was also taken for the measurement of plasma TNF-α with radioimmunology. Results: ① The apoptosis cells were less in SF group than in I/R group, and more than in control group (both P<0.05). ② The expression of Caspase-3 and fas protein in I/R group was all increased significantly than in control group and SF group(both P<0.01), but no differences between control group and SF group were found. ③ The expression of TNF-α in I/R group increased significantly than in control group and SF group (both P<0.05), but no differences were found between control group and SF group (P<0.01). ④ The injury of intestinal mucosal in SF group was alleviated than that of I/R group. Conclusion: Shenfu injection can reduce the apoptosis of intestinal mucosal epithelial cells during ischemia-reperfusion by restraining the expression of TNF-α, Fas and Caspase-3, thus to alleviate the injury of intestinal mucosal epithelial cells during ischemia-reperfusion.