Boric acid attenuates sepsis-induced cardiac injury through TLR4/mTOR modulation.

Boric acid (BA) has been reported to exert antioxidant and anti-inflammatory effects in various experimental settings; however, its role in sepsis-associated myocardial injury and the underlying molecular mechanisms remain incompletely understood. Polymicrobial infections cause severe organ damage and are associated with increased mortality in both neonatal and adult patients. In this study, we aimed to investigate the cardioprotective effects of BA and to explore its potential molecular mechanisms against myocardial injury in a cecal ligation and puncture (CLP)-induced sepsis model.Sprague-Dawley male rats were randomly assigned to Control, CLP, boric acid-treated (50 and 120 mg/kg), and boric acid + CLP groups, and BA was administered by oral gavage 1 h prior to CLP induction.Twenty-four hours after CLP, heart samples were collected. We investigated heart injury in terms of oxidative stress, inflammatory response, and also analyzed the activity of mTOR and vascular damage, which regulate cell metabolism and immunity. Furthermore, we evaluated caspase-3 gene expression in myocardial tissue by qRT-PCR. In vivo, BA treatment dose-dependently decreased myocardial oxidative stress markers (↓TOS), inflammatory mediators (↓TNF-α, ↓IL-1β), vascular adhesion molecules (↓VCAM-1, ↓ICAM-1), and myocardial TLR4 and mTOR expression, while increasing antioxidant capacity (↑TAC) and preserving cardiac tissue architecture. In addition, BA upregulated the anti-apoptotic protein Bcl-2 and suppressed caspase-3 gene expression in the heart tissues of CLP rats. The protective effects were more pronounced at the higher dose (120 mg/kg) compared with the lower dose (50 mg/kg). Overall, these findings suggest that BA attenuates sepsis-induced myocardial injury by modulating oxidative stress, inflammation, apoptosis, and vascular responses, potentially through regulation of the TLR4/mTOR signaling pathway.