中文摘要：

目的 观察苓桂术甘汤含药血清对脂多糖诱导的大鼠原代心肌细胞IKK/IκB/NF-κB信号通路相关蛋白表达的影响,探讨其保护心肌细胞的分子机制。方法 采用差速贴壁法和化学抑制法分离大鼠原代心肌细胞,分别设正常对照组、模型组、正常血清对照组、苓桂术甘汤含药血清（5%、10%、20%）组。通过脂多糖诱导复制心肌细胞损伤模型,检测含药血清预处理后心肌细胞NF-κBp65、IKK-β、IκB-α和p-IκBα蛋白表达,NF-κBp65核移位情况,TNF-α、IL-1β和IL-6的含量变化。结果 与正常对照组比较,模型组和正常血清对照组心肌细胞NF-κBp65、p-IκBα和心肌细胞核内NF-κBp65蛋白表达增加（P〈0.01）,心肌细胞IKK-β、IκB-α蛋白表达降低（P〈0.01）,细胞上清液IL-1β、IL-6和TNF-α含量升高（P〈0.01）;与模型组比较,苓桂术甘汤5%、10%、20%浓度含药血清组心肌细胞NF-κBp65、p-IκBα和心肌细胞核内NF-κBp65蛋白表达降低（P〈0.05）,心肌细胞IKK-β、IκB-α蛋白表达增加（P〈0.05）,细胞上清液IL-1β、IL-6和TNF-α含量降低（P〈0.05）,且干预效应与苓桂术甘汤含药血清呈浓度依赖趋势。结论 苓桂术甘汤可调节IKK/IκB/NF-κB信号通路相关蛋白表达,干预下游靶分子的转录调控,有效抑制细胞因子的过度激活。

英文摘要：

Objective To observe the effect of Linggui Zhugan Decoction （LZD） containing serum on the expressions of related proteins in IKK/IκB/NF-κB signaling pathways in lipopolysaccharide （LPS）-induced primary cardiomyocyte injury model rats, and to study its molecular mechanism for protecting cardiomyocytes. Methods Primary cardiomyocytes were isolated by differential wall adherence and chemical inhibition methods. Cardiomyocytes were then subdivided into normal control group, model group, normal serum control group, and LZD containing serum groups （5%, 10%, 20%）. The cardiomyocyte injury model was induced by LPS. Protein expressions of NF-κBp65, IKK-β, IκB-α, and p-IκBot were detected in cardiomyocytes after treated by LZD containing serums. Nuclear translocation of NF- κBp65 was observed. And the contents of TNF-α, IL-1β, and IL-6 in culture supernatant were analyzed. Results Compared with the normal control group, protein expressions of NF-κBp65 and p-IκBα in car- diomyocytes, and endonuclear NF-κBp65 protein expressions all increased （P 〈0.01 ）, protein expressions of IKK-β and IκB-β decreased in cardiomyocytes （P 〈0.01 ） ; contents of TNF-α, IL-1β, and IL-6 in-creased （P 〈0.01） in the model group and the normal serum control group. Compared with the model group, protein expressions of NF-κBp65 and p-IκBα in cardiomyocytes, and endonuclear NF-κBp65 protein expression all decreased （P 〈 0.05）, protein expressions of IκK-β and IκB-α increased in cardiomyocytes （P 〈0.05）; contents of TNF-α, IL-1β, and IL-6 decreased （P 〈0.01 ） in the 3 LZD containing serum groups. Besides, intervention effects showed dose-dependent relation to concentrations of LZD. Conclusion LZD could regulate IKK/I-κB/NF-κB signaling pathways related protein expressions, intervene transcriptional control of IKK/I-κB/NF-κB downstream target molecules, and effectively inhibit excessive activation of cytokines.