Honokiol Ameliorates Post-Myocardial Infarction Heart Failure Through Ucp3-Mediated Reactive Oxygen Species Inhibition

• DOI: 10.3389/fphar.2022.811682
• Publication Date: 2022-02-21T06:51:25Z
• Authors: Jianyu Liu; Minghai Tang; Tao Li; Zhengying Su; Zejiang Zhu; Caixia Dou; Yan Liu; Heying Pei; Jianhong Yang; Haoyu Ye; Lijuan Chen
• Keywords: UCP3; Mitochondrial ROS

Post-myocardial infarction heart failure (post-MI HF) is one of the leading global causes death, and current prevention treatment methods still cannot avoid increasing incidence. Honokiol (HK) has previously been reported to improve myocardial ischemia/reperfusion injury reverse hypertrophy by activating Sirt1 Sirt3. We suspect that HK may also have a therapeutic effect on post-MI HF. In this study, we aimed investigate efficacy mechanism in found inhibited reactive oxygen species (ROS) production, reduced fibrosis, improved cardiac function mice after MI. abnormality mitochondrial membrane potential (MMP) apoptosis cardiomyocytes caused peroxide neonatal cardiomyocytes. RNAseq results revealed restored transcriptome changes certain extent significantly enhanced expression inner uncoupling protein isoform 3 (Ucp3), inhibits production ROS, protects cardiomyocytes, relieves (MI). with impaired Ucp3 expression, protect against damage peroxide. More importantly, knockout mice, did not change increase ROS level Taken together, our suggest can cardioprotective maintain MMP, thereby inhibiting MI ameliorating failure.