Protective role of TRIM16/Nrf2 signaling pathway in septic cardiomyopathy

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.