活血通腑优化方对实验性肠粘连大鼠的保护作用

Protective Effect of Huoxuetongfuyouhuafang on the Rats Ankylenteron

目的:观察活血通腑优化方对实验性肠粘连的防治效果。通过对大鼠血清IL-6、IL-1β、TNF-α及腹腔液中转化生长因子-β_1和结缔组织生长因子的蛋白含量的检测,探讨其对肠粘连防治作用的机理。方法:SD大鼠随机分为6组:正常组、模型组、四磨汤组,活血通腑优化方低、中、高剂量组;每组10只。除正常对照组外,其余各组大鼠均制备肠粘连模型。正常组和模型组灌胃生理盐水。活血通腑优化方低、中、高剂量组在造模后,灌胃给予活血通腑优化方(0.65、1.3、2.6 g/100 g),连续给药10 d。四磨汤组灌服1 mL/100 g的四磨汤,连续给药10 d。各组大鼠于术后第11 d麻醉取下腔静脉血,ELISA法测定血清IL-6、IL-1β和TNF-α含量;并取腹腔液检测TGF-β_1和CTGF的含量,同时记录大鼠肠粘连级别。结果:与正常组相比,模型组血清IL-1β和TNF-α含量增高(P<0.01),腹腔液中TGF-β_1和CTGF的含量也升高(P<0.01)。与模型组相比,活血通腑优化方低、中、高剂量组的肠粘连程度明显减轻(P<0.05),血清IL-1β和TNF-α含量明显降低(P<0.05),腹腔液中TGF-β_1和CTGF的含量明显下降(P<0.05)。结论:活血通腑优化方可剂量依赖的减轻肠粘连的程度,对肠粘连具有防治作用。其作用可能是通过下调炎性因子TNF-α、IL-1β的表达,同时与抑制TGF-β_1信号通路有关。

To investigate the protective effect of Huoxuetongfuyouhuafang on rat ankylen-teron. Methods： Sixty SD rats were randomly divided into 6 groups： normal control group, model group, Simo Soup group, and low- medium- and high- dose Huoxuetongfuyouhuafang groups. Except the normal control group, the rats in the other groups were induced ankylenteron. Intragastric administration of saline was administered to the rats in the normal control group and the model group. The low- medium- and high- dose Huoxuetongfuyouhuafang groups accepted intragastric administration by the doses 0.65, 1.3 and 2.6 g/100 g, respectively, for 10 days. On the 11th day after surgery, the blood serum and the adhesion tissue of each group were collected. The levels of interleukin-1β （IL-1β）, interleukin-6 （IL-6）, tumor necrosis factor-α （TNF-α） in blood serum and the contents of TGF-β1 and CTGF in the peritoneal fluid were all measured by ELISA kits. Grades of intestinal adhesion were ranked by macroscopic observation. Results： Huoxuetongfuyouhuafang can significantly relieved the experimental intestinal adhesion and de-creased the levels of IL-1β, IL-6 and TNF-α in blood serum and TGF-β1 and CTGF in the peritoneal fluid significantly （P〈0.05）. Conclusion： Huoxuetongfuyouhuafang can effectively prevent the formation of postoperative ankylenteron by inhibiting the expression of inflammatory cytokines and depressing the levels of TGF-β1 and CTGF.