| Literature DB >> 36160853 |
Xuqing Li1,2, Li Wang1,2, Xinwang Ying1,2, Yujun Zheng1,2, Qianqian Tan1,2, Xiaolan Yu1,2, Jiahong Gong1,2, Ming Li1,2, Xiaofeng Deng3, Guanhu Yang1,2, Shengcun Li1,2,4, Songhe Jiang1,2.
Abstract
Electroacupuncture (EA) has both anti-inflammatory and cardio-protective effects. Activation of calpain pathway is involved in several myocardiopathy. In sepsis, the role of calpain-2-regulated STAT3 in cardio-protective mechanism of electroacupuncture remains unclear. In this study, we aimed to elucidate the mechanism by which electroacupuncture reduces cardiac inflammation and apoptosis and improves cardiac function during sepsis. Electroacupuncture pretreatment for 7 days was applied in septic cardiomyopathy model induced by lipopolysaccharide (LPS). lipopolysaccharide-induced sepsis was associated with a dramatically systemic inflammation and cardiac dysfunction, which was alleviated by electroacupuncture pre-treatment. Lipopolysaccharide resulted in increases of pro-inflammatory factors (TNF-α,IL1βand IL-6) and apoptosis (TUNEL staining and BAX/Bcl2) via activation of calpain-2/STAT3 pathway.Electroacupuncture pre-treatment inhibited LPS-induced activation of cardiac calpain-2/STAT3 signalling and ameliorated inflammatory and apoptosis. Additionally, inhibition of calpain-2 expression using the corresponding siRNA decreased the Phosphorylation of STAT3,pro-inflammatory factors and apoptosis in lipopolysaccharide- treated cardiomyocytes, confirming that calpain-2 activated p-STAT3 participate in septic cardiomyopathy. Furthermore, suppression of STAT3 by stattic enhanced anti-inflammatory and anti-apoptosis effects of electroacupuncture. These findings reveal mechanisms of electroacupuncture preconditioning protection against cardiac inflammation and apoptosis in sepsis mouse via calpain-2/STAT3 pathway and may provide novel targets for clinical treatments of the sepsis-induced cardiac dysfunction.Entities:
Keywords: calpain-2; electroacupuncture; heart; myocardial inflammation; stat3
Year: 2022 PMID: 36160853 PMCID: PMC9489935 DOI: 10.3389/fphys.2022.961909
Source DB: PubMed Journal: Front Physiol ISSN: 1664-042X Impact factor: 4.755