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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 investigate the effect of Panzhiyan mixture and Shanning on serum interleukin 6 (IL 6) in rats with severe acute pancreatitis (SAP). Methods Ninety-six healthy Wistar rats were randomly divided into negative control group (NC group), severe acute pancreatitis model group (SAP group), Shanning treatment group (SH group) and pancreatitis mixture treatment group (YH group). A severe acute pancreatitis model was made by retrograde injection of 5% sodium taurocholate into the biliary and pancreatic ducts of rats, and the two treatment groups were treated with Pancreatitis mixture and Shanning. The rats in each group were sacrificed at 12, 24, and 48 h. Serum IL 6 levels were measured. The pathological changes of pancreas, light microscopy, and electron microscopy were observed. Results Compared with the NC group, the serum IL 6 levels in the SAP rats were significantly higher at the same time (P<0.01). Serum IL-6 levels began to decrease significantly at 24 h after treatment with Panzhi Mixture (P<0. 01), and serum IL 6 levels began to decrease at 12 h after Shanning treatment (P<0.01), but there was no significant difference at 48 h (P<0.01). >0. 05). The pathological changes of the pancreas were observed by light microscope and electron microscope. The pathological changes in the YH group and the SH group were similar, and all were significantly reduced compared with the SAP group. Conclusion IL-6 plays a promoting role in the pathogenesis of severe acute pancreatitis in rats. The combination of Pancreatitis and Shanning has a good therapeutic effect on animals with severe acute pancreatitis. One of the mechanisms may be to block the production of IL-6 or inhibit its activity, thus reducing the excessive inflammation.