Abstract

Cytokine-induced apoptosis inhibitor 1 is a protein involved in controlling apoptosis and programmed cell death. The role of cytokine-induced apoptosis inhibitor 1 against lipopolysaccharide-induced myocardial damage remains unclear. The research aimed to assess cytokine-induced apoptosis inhibitor 1 protective function against lipopolysaccharide-induced myocardial damage and the mechanism underlying it. In vivo and in vitro sepsis models were developed using lipopolysaccharide-induced male C57BL/6 mice and H9c2 cardiomyocytes. Our study found that lipopolysaccharide-induced myocardial tissue in mice decreased cytokine-induced apoptosis inhibitor 1 expression while elevating interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha levels. Moreover, cytokine-induced apoptosis inhibitor 1 was also decreased in the lipopolysaccharide-induced H9c2 cardiomyocytes. Overexpression of cytokine-induced apoptosis inhibitor 1 in the lipopolysaccharide+LV-cytokine-induced apoptosis inhibitor 1 group cells inhibited cell proliferation, the apoptotic rate, cellular reactive oxygen species, and oxidative stress. The cytokine-induced apoptosis inhibitor 1 overexpression also remarkably attenuated the release of inflammatory cytokines. Furthermore, cytokine-induced apoptosis inhibitor 1 overexpression potentially increases silent information regulator 1 expression and suppresses thioredoxin interacting protein, NOD-like receptor protein 3 and caspase-1 p10 protein expressions in the lipopolysaccharide+LV-cytokine-induced apoptosis inhibitor 1 group cells. These findings indicate that cytokine-induced apoptosis inhibitor 1 potentially improves lipopolysaccharide-induced myocardial injury by attenuating silent information regulator 1-dependent NOD-like receptor protein 3 inflammasome activation, providing a therapeutic strategy to prevent and treat lipopolysaccharide -induced myocardial injury.