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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 clarify the role of interleukin-6 (IL-6) in acute pancreatitis in mice and its mechanism. Methods: Acute pancreatitis was induced in mice by ligation of pancreatic duct; pancreatic acinar cells were isolated from mice. The cytokines in pancreatic tissue or acinar cell lysate were detected by ELISA. The expression of IL-6 or ERK in tissues or cells was detected by western blot. Results: IL-6 concentration was significantly increased in pancreatic tissue and acinar cells (P <0.05). In isolated primary murine acinar cells, TNF-alpha stimulation increased IL-6 release (P <0.05); in the meantime, IL-6 stimulation increased the release of other proinflammatory cytokines, both of which involved ERK MAP kinase pathway. The flavonoid luteolin inhibits the release of interleukin-6 (IL-6) and human macrophage-activating protein-1 (CCL2 / MCP-1) by IL-6 stimulation. Finally, it was further confirmed that IL-6 activates ERK in human pancreatic tissue. Conclusion: IL-6 is increased in acute pancreatitis, activating the inflammatory pathway and aggravating acute pancreatitis.