Taurine Alleviates Sepsis-Induced Myocardial Injury by Inhibiting NF-κB Pathway-Mediated Inflammation, Mitochondrial Dysfunction, and Apoptosis.

Abstract

Sepsis-induced cardiomyopathy (SICM) is a life-threatening complication characterized by cardiac dysfunction, inflammation, oxidative stress, and mitochondrial impairment, with limited therapeutic options. Taurine, a naturally occurring amino acid with known anti-inflammatory and mitochondrial-stabilizing properties, may offer therapeutic benefits. However, its role in SICM is not well defined. This study aimed to evaluate the protective effects of taurine against SICM and elucidate its underlying mechanisms. A murine model of SICM was established via cecal ligation and puncture (CLP), and AC16 cardiomyocytes were stimulated with lipopolysaccharide (LPS) to mimic septic injury in vitro. Cardiac function was assessed by echocardiography; inflammatory cytokines and cardiac injury markers were measured via ELISA. Mitochondrial integrity and function were evaluated using transmission electron microscopy (TEM), oxygen consumption rate (OCR), and mitochondrial membrane potential (MMP). Apoptosis was analyzed by TUNEL staining, flow cytometry, and Western blot. Rescue experiments using an NF-κB activator were conducted to validate pathway involvement. The results showed that taurine treatment significantly improved cardiac function and survival rates in SICM mice, attenuated myocardial inflammation and oxidative stress, restored mitochondrial structure and function, and suppressed apoptosis. These beneficial effects were reversed upon NF-κB activation, indicating that taurine exerts its cardioprotective role primarily through inhibition of the NF-κB signaling pathway. In conclusion, this study provides the first evidence that taurine protects against SICM by alleviating NF-κB-driven inflammation, oxidative stress, mitochondrial dysfunction, and apoptosis, suggesting its potential as a therapeutic agent for sepsis-induced cardiac injury.