TRIM16/Nrf2信号通路在脓毒症心肌病中的重要作用

    Protective role of TRIM16/Nrf2 signaling pathway in septic cardiomyopathy

      摘要
    • 摘要:
      目的 明确TRIM16在脓毒症心肌损伤中的作用及机制。
      方法 将小鼠随机分为2组：Sham组和CLP（盲肠结扎穿孔）组；体外实验分组：对照组（PBS）、PBS-TRIM16处理组、LPS组、LPS-TRIM16保护组、TRIM16 siRNA组、LPS-TRIM16 siRNA组、LPS-Nrf2 siRNA组和LPS-TRIM16-Nrf2 siRNA组。采用ELISA、Western blot、DCFH-DA染色等技术检测炎性因子释放及氧化应激水平、CCK-8检测细胞活力。
      结果 与对照组相比，脓毒症心肌病小鼠心肌组织及LPS诱导的nmCMs细胞中TRIM16的蛋白表达水平显著升高（P<0.05），氧化应激显著增加（P<0.01），同时可见Nrf2蛋白表达量显著降低及NLRP3水平显著增加（P<0.05，P<0.01）。TRIM16处理后，可通过增加Nrf2蛋白表达水平而部分缓解LPS诱导的nmCMs细胞损伤。在给予siRNA抑制Nrf2表达后，TRIM16的保护作用被显著减弱，同时氧化应激水平显著增加。
      结论 TRIM16可通过激活Nrf2转导减轻脓毒症诱导的心肌细胞毒性。

       

      Abstract:
      AIM To clarify the role and mechanism of TRIM16 in septic cardiomyopathy.
      METHODS Mice were randomly divided into the following groups: PBS group, PBS-TRIM16 group, LPS group, LPS-TRIM16 group, TRIM16 siRNA group, LPS-TRIM16 siRNA group, LPS-Nrf2 siRNA group and LPS-TRIM16-Nrf2 siRNA group. The release of inflammatory factors and oxidative stress levels were determined by ELISA, Western blot and DCFH-DA staining, and cell viability was determined by CCK-8.
      RESULTS Compared with the control group, myocardial tissue from mice with septic cardiomyopathy and LPS-induced nmCMs cells showed a significant increase in TRIM16 protein expression (P<0.05) and a significant increase in oxidative stress (P<0.01), as well as a significant decrease in Nrf2 protein expression and a significant increase in NLRP3 (P<0.05, P<0.01). TRIM16 treatment partially ameliorated LPS-induced nmCMs cell injury by increasing the level of Nrf2 protein expression. The protective effect of TRIM16 was significantly reduced, while the level of oxidative stress was significantly increased after Nrf2 inhibition.
      CONCLUSION TRIM16 mitigates LPS-induced cardiotoxicity via activating Nrf2 signaling.

       

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