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目的:探讨参附注射液(SFI)对大鼠肠缺血-再灌注(I/R)引起的远隔器官肝脏损伤的保护作用。方法:采用钳闭大鼠肠系膜上动脉复制缺血再灌注模型。40只健康♂Wistar大鼠随机分为4组(n=10):假手术组(Sham组);肠I/R组(II/R组);低剂量参附注射液处理组(SF-5组,5mL.kg-1);高剂量参附注射液处理组(SF-10组,10mL.kg-1)。通过夹闭肠系膜上动脉60min,再灌注120min,建立肠I/R损伤模型。SFI组于再灌注前腹腔注射SFI,假手术组不阻断肠系膜上动脉血流。观察各组大鼠肠道丙二醛(MDA)水平,肝组织MDA、肿瘤坏死因子-α(TNF-α)水平,血清谷丙转氨酶(ALT)、谷草转氨酶(AST)水平,及肠道、肝脏组织H-E染色,肝脏核因子-κB(NF-κB)Western Blot分析。结果:II/R组肠组织MDA水平、肝组织中MDA水平、TNF-α水平及血清ALT、AST水平明显高于假手术组(P<0.05),NF-κB表达明显高于假手术组(P<0.05),镜检发现肠、肝组织有明显组织形态学损伤。与II/R组比较,SFI能够降低肠组织MDA水平、肝组织中MDA水平和TNF-α水平及血清ALT、AST水平(P<0.05);减少肝组织NF-κB表达(P<0.05);减轻肝脏组织形态学损伤。结论:SFI通过减少肝组织NF-κB激活,在肠I/R引起的肝脏损伤中发挥保护作用。
Objective: To investigate the protective effect of Shenfu injection (SFI) on hepatic injury of distal organs caused by intestinal ischemia-reperfusion (I/R) in rats. Methods: The model of ischemia-reperfusion injury was established by clamping the rat superior mesenteric artery. Forty healthy Wistar rats were randomly divided into 4 groups (n=10): Sham group (Sham group); Intestinal I/R group (II/R group); Low-dose Shenfu injection group (SF-5) Group, 5mL.kg-1); high-dose Shenfu injection treatment group (SF-10 group, 10mL.kg-1). The intestinal I/R injury model was established by clamping the superior mesenteric artery for 60 min and reperfusion for 120 min. In the SFI group, SFI was injected intraperitoneally before reperfusion, and the sham group did not block the blood flow of the superior mesenteric artery. The levels of malondialdehyde (MDA) in the intestine, the levels of MDA and TNF-α in liver tissue, the level of serum ALT, AST, and the intestinal tract were observed. Liver tissue HE staining, liver nuclear factor-κB (NF-κB) Western Blot analysis. Results: Intestinal tissue MDA levels, liver tissue MDA levels, TNF-α levels, serum ALT, AST levels in II/R group were significantly higher than those in sham operation group (P<0.05), and NF-κB expression was significantly higher than that in sham operation group ( P<0.05). Microscopic examination revealed significant histomorphological damage in the intestine and liver tissues. Compared with the II/R group, SFI was able to reduce MDA level, MDA level and TNF-α level in liver tissue, serum ALT and AST levels (P<0.05), and reduce NF-κB expression in liver tissue (P<0.05). Reduce liver tissue morphological damage. CONCLUSIONS: SFI plays a protective role in intestinal I/R-induced liver injury by reducing NF-κB activation in the liver.