白细胞介素-6在急性胰腺炎中的作用及其机制研究

The Interleukin-6 is Involved in Acute Pancreatic in Mice and Its Mechanisms

目的:明确白细胞介素-6(IL-6)在小鼠急性胰腺炎中的作用及其机制研究。方法:通过胰胆管结扎的方法诱导小鼠急性胰腺炎;分离小鼠胰腺腺泡细胞。采用ELISA方法检测胰腺组织或腺泡细胞裂解物中的细胞因子;通过western blot分析检测组织或细胞中IL-6或ERK表达。结果:IL-6浓度在胰腺组织和腺泡细胞中显著增加(P<0.05)。在离体原代小鼠腺泡细胞,TNF-α刺激增加IL-6释放(P<0.05);与此同时,IL-6刺激可增加其它促炎性细胞因子的释放,两者都涉及ERK MAP激酶通路。黄酮类化合物木犀草素抑制IL-6刺激引起白细胞介素-6(IL-6)和人巨嗜细胞激活蛋白-1(CCL2/MCP-1)释放。最后进一步证实,IL-6激活人胰腺组织中的ERK。结论:IL-6在急性胰腺炎中增加,激活炎症通路并加重急性胰腺炎。

Objective： To investigate whether interleukin-6（IL-6） exacerbates acute pancreatic inflammation in mice and its mechanisms. Methods： The pancreatic acinar cells were isolated from mice with duct ligation-induced acute pancreatitis. ELISA was used to measure cytokines in pancreas tissue or acinar cells lysates, and western blot analysis was applied to detect the expression of IL-6or ERK. Results： IL-6 concentration was increased in the pancreas and acinar cell（P〈0.05）. In isolated mouse pancreatic acinar cells,TNF-α stimulation increased IL-6 release while IL-6 stimulation increased release of proinflammatory cytokine, and both involved the ERK MAP kinase pathway. The flavonoid luteolin inhibited the release of IL-6-stimulated IL-6 and CCL2/MCP-1. Also, IL-6 activated ERK in human pancreatic tissue. Conclusion： IL-6 is induced in acute pancreatitis, activates acinar cell proinflammatory pathways and exacerbates acute pancreatic inflammation.