Melatonin Alleviates Cardiac Function in Sepsis-Caused Myocarditis via Maintenance of Mitochondrial Function

Liyang Chen; Qing Tian; Zhiguang Shi; Yu Qiu; Qiulun Lu; Chao Liu

doi:10.3389/fnut.2021.754235

Melatonin Alleviates Cardiac Function in Sepsis-Caused Myocarditis via Maintenance of Mitochondrial Function

Front Nutr. 2021 Oct 11:8:754235. doi: 10.3389/fnut.2021.754235. eCollection 2021.

Authors

Liyang Chen¹, Qing Tian², Zhiguang Shi¹, Yu Qiu³, Qiulun Lu¹, Chao Liu⁴

Affiliations

¹ Key Laboratory of Cardiovascular and Cerebrovascular Medicine, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, China.
² Intensive Care Unit of Wuhan Asia Heart Hospital, Wuhan, China.
³ Center for Molecular and Translational Medicine, Georgia State University, Atlanta, GA, United States.
⁴ Hubei Key Laboratory of Diabetes and Angiopathy, Hubei University of Science and Technology, Xianning, China.

Abstract

Melatonin (N-acetyl-5-methoxytryptamine) has been shown to have a cardioprotective effect against myocarditis. However, the mechanisms underlying the protective role of melatonin (MLT) in sepsis-induced myocarditis are yet to be revealed. In this study, MLT was administrated to mice, 14 days before cecal ligation puncture surgery. Echocardiography results showed that MLT alleviated cardiac dysfunction in sepsis-induced myocarditis. Furthermore, MLT reduced cardiac inflammation by inhibiting the expression of Il-1α, Il-1β, Il-6, and Mcp-1 messenger RNA (mRNA) levels. The RNA sequencing (RNA-seq) assays with heart tissues showed that MLT maintains the mitochondrial function in sepsis-caused myocarditis. Additionally, the production of reactive oxygen species (ROS) in heart tissues was suppressed by MLT. Taken together, in evaluating the therapeutic effect of MLT on sepsis-induced myocarditis, the results showed that MLT alleviated cardiac damage by regulating mitochondrial function and mitochondrial ROS.

Keywords: ROS; cardiac function; melatonin; mitochondria; sepsis-induced myocarditis.