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目的:探讨参附注射液(Shenfu injection,SFI)对重症急性胰腺炎(SAP)大鼠肠屏障功能障碍与二次打击的防护作用。方法:雄性Wistar大鼠54只,随机分为3组:SAP组(SAP,n=24),采用逆行十二指肠胰胆管注射5%牛黄胆酸钠溶液制备SAP大鼠模型;SAP+SFI组(n=24),建模前2h先给予SFI10ml/kg体质量腹腔注射;假手术组(SO,n=6)。建模成功后3、6、12、24h,分别取血液和小肠、胰腺、肺脏、肝脏标本。光镜下观察小肠组织病理改变,检测各时段血浆TNF-α、IL-6和二胺氧化酶(diam-ineoxidase,DAO)活性,以及相应时段胰腺、肺脏、肝脏中髓过氧化物酶(MPO)含量。结果:SAP组各时间点血液TNF-α、IL-6、DAO均较SO组显著升高(P<0.01),6～24h胰腺、肺脏、肝脏MPO较SO组显著升高(P<0.01);SAP+SFI组各时间点血液DAO、TNF-α和IL-6水平显著低于SAP组(P<0.05或P<0.01),6～24h胰腺、肺脏、肝脏MPO显著低于SAP组(P<0.05或P<0.01);SAP+SFI组建模后24h小肠病理组织改变较SAP组明显减轻。结论:SFI可防护SAP大鼠肠屏障功能障碍,并可减轻胰腺、肺脏、肝脏遭受二次打击的严重程度,其作用机制可能与减少中性粒细胞聚集、抑制促炎细胞因子TNF-α、IL-6相关。
Objective: To investigate the protective effect of Shenfu injection (SFI) on intestinal barrier dysfunction and secondary shock in rats with severe acute pancreatitis (SAP). Methods: Fifty-four male Wistar rats were randomly divided into three groups: SAP group (SAP, n = 24), SAP model was established by injecting 5% sodium taurocholate solution into the duodenum of the duodenum. (N = 24). The rats were injected intraperitoneally with SFI 10ml / kg body weight 2 hours before modeling. Sham operation group (SO, n = 6). 3,6,12,24 h after modeling, respectively, blood and small intestine, pancreas, lung, liver specimens. The pathological changes of small intestine were observed under light microscope. The levels of plasma TNF-α, IL-6 and DAO were measured at different time points. The levels of myeloperoxidase (MPO) in the pancreas, lung and liver )content. Results: Compared with SO group, the levels of TNF-α, IL-6 and DAO in SAP group increased significantly (P <0.01), and the levels of MPO in pancreas, lung and liver increased significantly ; The levels of DAO, TNF-α and IL-6 in blood in SAP + SFI group were significantly lower than those in SAP group (P <0.05 or P <0.01), and the MPO in pancreas, lung and liver at 6 ~ <0.05 or P <0.01). Compared with SAP group, the changes of pathological changes of intestinal tract in SAP + SFI group were significantly reduced 24 h after modeling. Conclusion: SFI can protect the intestinal barrier dysfunction in SAP rats and relieve the severity of secondary attacks on the pancreas, lung and liver. The mechanism may be related to reducing the aggregation of neutrophils, inhibiting the expression of pro-inflammatory cytokines TNF-α, IL-6 related.