Abstract
Cytokine-Induced Apoptosis Inhibitor 1 Protects Against Lipopolysaccharide-Induced Myocardial Injury by Suppressing SIRT1-Dependent NLRP3 Inflammasome Activation
Department of Nursing, Shanghai Pudong New Area Zhoupu Hospital (Shanghai Health Medical College Affiliated Zhoupu Hospital), Shanghai 201318, 1Department of Pharmacy, Sijing Hospital of Songjiang District, Songjiang, Shanghai 201601, China
Correspondence Address:
Nongzhang Xu, Department of Pharmacy, Sijing Hospital of Songjiang District, Songjiang, Shanghai 201601, China, E-mail: Long1983805@126.com
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.
Full-Text | PDF