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    基于ROS/JNK信号通路探讨红花黄色素对在冠心病心肌细胞焦亡的保护机制

    Exploring the protective mechanism of safflower yellow pigment on myocardial pyroptosis in coronary heart disease based on ROS/JNK signaling pathway

      摘要
    • 摘要:
      目的： 探究红花黄色素对冠心病（CHD）小鼠心肌组织ROS/c–Jun N–末端激酶（JNK）信号通路及心肌细胞焦亡的影响。
      方法： 选择10只C57BL/6J小鼠为对照组；选择30只18～22 g SPF级雄性ApoE–/–小鼠随机分为CHD组、红花黄色素组及JNK磷酸化抑制剂组(Urolithin B组)，每组10只。超声心动图检测左心室射血分数(LVEF)，左心室短轴缩短率（LVFS），HE染色检测心肌组织病理变化，Masson染色检测心肌组织纤维化水平，试剂盒检测ROS、IL–1β、IL–18含量，Western blotting检测心肌组织JNK、p–JNK、NLRP3及Caspase–1蛋白表达水平。
      结果： 与对照组比较，CHD组小鼠LVEF、LVFS减少（P ＜ 0.05），心肌纤维紊乱、断裂，心肌间隙可见胶原大量沉积，心肌组织中p–JNK、NLRP3、Caspase–1蛋白表达与ROS、IL–1β、IL–18水平增加（P ＜ 0.05）；与CHD组比较，红花黄色素组小鼠LVEF、LVFS增加，心肌纤维损伤改善，心肌间隙胶原沉积减少，心肌组织中p–JNK、NLRP3、Caspase–1蛋白表达与ROS、IL–1β、IL–18水平减少（P ＜ 0.05），Urolithin B组小鼠心肌组织NLRP3、Caspase–1蛋白表达与IL–1β、IL–18水平减少（P ＜ 0.05）。
      结论： 红花黄色素可改善CHD小鼠心功能及心肌组织病理损伤，下调心肌组织中ROS/JNK通路，并抑制心肌细胞焦亡。

       

      Abstract:
      Objective To investigate the effects of safflower yellow pigment on the ROS/c-Jun N-terminal kinase (JNK) signaling pathway and cardiomyocyte pyroptosis in myocardial tissue of coronary heart disease (CHD) mice.
      Methods Ten C57BL/6J mice were selected as the control group; thirty 18-22 g SPF male ApoE-/- mice were randomly divided into the CHD group, the safflower yellow pigment group, and the JNK phosphorylation inhibitor group (Urolithin B group), with 10 mice in each group. Echocardiography was used to measure left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS). HE staining was used to detect pathological changes in myocardial tissue, Masson staining was used to detect the level of fibrosis in myocardial tissue, and reagent kits were used to detect the levels of ROS, IL-1β, and IL-18. Western blotting was used to detect the expression levels of JNK, p-JNK, NLRP3, and Caspase-1 proteins in myocardial tissue.
      Results Compared with the control group, the LVEF and LVFS of mice in the CHD group decreased (P ＜ 0.05), myocardial fibers were disordered and fractured, and a large amount of collagen deposition was observed in the myocardial interstitium. The expression levels of p-JNK, NLRP3, Caspase-1 proteins and the levels of ROS, IL-1β, and IL-18 in myocardial tissue increased (P ＜ 0.05). Compared with the CHD group, the LVEF and LVFS of mice in the safflower yellow pigment group increased, myocardial fiber damage improved, collagen deposition in the myocardial interstitium decreased, and the expression levels of p-JNK, NLRP3, Caspase-1 proteins and the levels of ROS, IL-1β, and IL-18 in myocardial tissue decreased (P ＜ 0.05). In the Urolithin B group, the expression levels of NLRP3 and Caspase-1 proteins and the levels of IL-1β and IL-18 in myocardial tissue decreased (P ＜ 0.05).
      Conclusions Safflower yellow pigment can improve cardiac function and myocardial tissue pathological damage in CHD mice, downregulate the ROS/JNK pathway in myocardial tissue, and inhibit cardiomyocyte pyroptosis.

       

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