目的研究茶多酚(TP)对大鼠肠缺血再灌注(I/R)肝损伤的保护作用及其可能的作用机制,为其临床新用途提供实验依据。方法大鼠随机分为模型组、假手术组及TP(100.0、50.0、25.0、12.5mg/kg)组,通过夹闭肠系膜上动脉60min、再灌注120min,建立肠I/R损伤模型。于缺血前20min舌下iv药物,假手术组仅分离不夹闭肠系膜上动脉。再灌120min后,各组取血及肝组织,测定血清及肝组织中SOD活力、MDA和NO水平,光镜下观察肝组织形态学改变。结果与假手术组相比,肠I/R损伤后,血清及肝组织中的SOD活力降低,MDA、NO水平升高,镜检发现肝有明显组织形态学损伤。与模型组相比,TP呈剂量依赖性增强SOD活力,降低MDA及NO水平,减轻肝组织形态学损伤。结论TP对肠I/R所致肝损伤有显著的剂量依赖性的保护作用,可能与其自由基清除作用、减轻中性粒细胞聚集及活化、抑制大量NO释放有关。

Objective To investigate the protective effects of tea polyphenols (TP) on intestinal ischemia reperfusion (I/R) induced injury of liver in rats and possible action mechanism, so as to provide preclinical pharmacological basis for its new clinical uses. Methods Rats were randomly divided into six groups: Sham group, model group, and TP (100.0, 50.0, 25.0, and 12.5 mg/kg) groups. Intestinal I/R model was established by clamping superior mesenteric artery for 60 min and reperfusing for 120 min. TP was administered by sublingual vein at 20 min before ischemia. In Sham group, superior mesenteric artery was only isolated without clamping. Blood samples and liver tissue samples were collected after reperfusion lasting 120 min. SOD activity, MDA and NO levels in serum and liver tissue were determined. Histomorphology changes of liver tissue were observed with light microscope. Results Compared with Sham group, after intestinal I/R injury, activity of SOD was decreased, while the levels of MDA and NO was increased in serum and liver tissue. At the same time, histomorphology of liver was destroyed obviously, as seen by light microscope. In comparison with model group, TP could dose-dependently increase SOD activity, decrease MDA and NO levels in serum and liver tissue. Also, TP could dose-dependently attenuate liver tissue injury, as evidenced by microscopic examination of histomorphology. Conclusion TP can dose-dependently protect liver significantly and attenuate intestinal I/R injury. These protective effects are related to their anti-free-radical actions with diminishing the aggregation and activation of polymorphonuclear neutrophils (PMN) and inhibiting the release of NO.