巴马汀通过抑制NF-κB信号通路改善CLP诱导的脓毒症

Palmatine ameliorates CLP-induced sepsis via inhibition of NF-κB signaling pathway

目的 探究巴马汀(PAL)对盲肠结扎穿刺法(CLP)诱导的脓毒症的干预作用及机制。方法 构建CLP诱导的脓毒症模型小鼠,HE染色观察CLP小鼠肺组织形态,ELISA法检测CLP小鼠血清和脾脏中IL-1β、IL-6、TNF-α水平,Q-PCR检测CLP小鼠脾脏IL-1β、IL-6、TNF-α mRNA表达,Western blot法检测CLP小鼠脾脏组织细胞核NF-κB蛋白表达。结果 PAL能提高CLP脓毒症小鼠的生存率,明显改善小鼠肺损伤,显著降低CLP小鼠血清和脾脏中IL-1β、IL-6、TNF-α表达水平(P <0.01)。Western blot结果显示,PAL各剂量组小鼠脾脏中细胞核NF-κB蛋白表达明显下调且呈一定的剂量依赖性。结论 PAL可以抑制CLP诱导的促炎因子释放,可能通过抑制NF-κB信号通路起到改善CLP诱导的脓毒症的作用。

Objective To determine the intervention and mechanism of palmatine(PAL)on cecal ligation and perforation(CLP)-induced sepsis.Methods CLP-induced sepsis mouse model was constructed.The lung morphology of CLP mice was observed by HE staining.The levels of IL-1β,IL-6 and TNF-αin the serum and the spleen of CLP mice were detected by ELISA.The mRNA expressions of IL-1β,IL-6 and TNF-αin the spleen of CLP mice were detected by Q-PCR.Western blot was used to detect the expression of nuclear NF-κB protein in the spleen tissues of CLP mice.Results PAL improved the survival rate of mice with CLP sepsis,significantly improved the lung injury of the mice,and reduced the expression levels of IL-1β,IL-6 and TNF-αin the serum and the spleen of CLP mice.Western blot showed that the expression of nuclear NF-κB protein in the spleens of the PAL groups was significantly down-regulated in a dose-dependent manner.Conclusion PAL can inhibit the release of proinflammatory factors induced by CLP,and plays a role in improving CLP-induced sepsis by inhibiting NF-κB signaling pathway.