胰炎合剂对重症急性胰腺炎大鼠血清白细胞介素-6的影响

Influence of Yiyanheji on serum interleukin-6 in severe acute pancreatitis rats

目的 探讨胰炎合剂、善宁对重症急性胰腺炎(SAP)大鼠血清白细胞介素6 (IL 6 )的影响。方法 将96只健康Wistar大鼠随机分为阴性对照组(NC组)、重症急性胰腺炎模型组(SAP组)、善宁治疗组(SH组)和胰炎合剂治疗组(YH组)。采用向大鼠胆胰管内逆行注射5%牛磺胆酸钠的方法制成重症急性胰腺炎模型,用胰炎合剂和善宁对两治疗组分别进行治疗。于12、24、48h处死各组大鼠,检测血清IL 6含量,观察胰腺大体、光镜和电镜的病理变化。结果 与NC组比较,SAP大鼠各相同时点血清IL 6水平均明显升高(均为P<0. 01)。胰炎合剂治疗后24h血清IL 6水平开始明显下降(P<0. 01),善宁治疗后12h血清IL 6水平开始明显下降(P<0. 01),而于48h差异无显著性(P>0. 05)。胰腺组织大体、光镜及电镜观察,YH组与SH组的病理变化相似,均较SAP组明显减轻。结论 IL 6在大鼠重症急性胰腺炎的发病中发挥了促进作用。胰炎合剂与善宁对重症急性胰腺炎动物具有较好的治疗作用,其机制之一可能是通过阻断IL 6的生成或抑制其活性,减轻了过度炎症反应。

Objective To study the changes of serum interleukin-6 (IL-6) in rats with severe acute pancreatitis (SAP) when treated with Yiyanheji and Sandostain.Methods 96 healthy Wistar rats were randomly divided into 4 groups: negative control group (NC group),severe acute pancreatitis (SAP group) group,Sandostain group (SH group) and Yiyanheji group (YH group).Animal models of SAP were induced by retrograde injection of 5% sodium taurocholate into the pancreatic duct in rats.SH group and YH group were treated with Sandostain and Yiyanheji respectively.IL-6 level was measured and pancreatic specimen was observed by macroscopy and optical microscopy and electron microscopy at 12h,24h and 48h when the rats were killed.Results After SAP was induced,the serum IL-6 level of the rats increased significantly (P<0.01) which was decreasing 12h after the group was treated with Sandostain (P<0.01) and 24h after the group was treated with Yiyanheji (P<0.01).There was significant difference in the serum IL-6 level between YH and SH group at 12h and 24h(P<0.01) but no significant difference at 48h(P>0.05).YH group presented the same pathological changes as SH group under the observation of macroscopy,optical microscopy and electron microscopy,but both group showed obvious amelioration as compared with SAP group.Conclusion IL-6 can promote the onset of SAP.Yiyanheji and Sandostain may better treat SAP in rats,with one of the mechanisms of alleviating excessive inflammatory reaction by inhibiting the production of IL-6 or reducing its activity.