Sevoflurane, as opposed to pentobarbital anesthesia, attenuates LPS-induced myocardial injury by up-regulating TAF1D.

Septic cardiomyopathy (SCM) is a prevalent and severe complication associated with sepsis. This study explores the effects of sevoflurane and pentobarbital on lipopolysaccharide (LPS) -induced SCM and elucidates underlying mechanisms. The SCM model was established using an intraperitoneal injection of 10 mg/kg LPS. Pentobarbital and sevoflurane were administered thirty minutes post-model establishment. Following the echocardiographic assessment, mice were euthanized 24 h after the modeling, and cardiac samples were collected. Gene sequencing and western blot were utilized to identify potential hub genes and signaling pathways. Sevoflurane markedly reduced LPS-induced myocardial injury and cardiac dysfunction compared to the pentobarbital intervention. Transcriptome sequencing revealed that numerous genes exhibited differential expression following intervention with sevoflurane and pentobarbital, with predominant enrichment in the signaling pathways, such as the extracellular region and matrix, tumor necrosis factor (TNF), and p53 signaling. Sevoflurane significantly induced TATA-box binding protein-associated factor, RNA polymerase I subunit D (TAF1D) expression and attenuated cardiomyocyte death, oxidative stress, and the secretion of IL-6 and TNF-α compared to the pentobarbital group (p < 0.05). Furthermore, oe-TAF1D significantly exacerbated cardiomyocyte death, oxidative stress, and inflammatory responses, which were alleviated with si-TAF1D (p < 0.05). Sevoflurane mitigates sepsis-induced cell death, oxidative stress, and inflammatory responses by up-regulating TAF1D, consequently diminishing cardiac injury and preserving cardiac function.