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Original Article

Korean J Physiol Pharmacol 2022; 26(6): 511-518

Published online November 1, 2022

Copyright © Korean J Physiol Pharmacol.

Neogambogic acid relieves myocardial injury induced by sepsis via p38 MAPK/NF-κB pathway

Wei Fu#, Xiaowei Fang#, Lidong Wu*, Weijuan Hu, and Tao Yang

Department of Emergency, Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330000, China

Correspondence to:Lidong Wu

#These authors contributed equally to this work.

Author contributions: W.F. and X.F. conceptualization, Methodology, Completed, and Writing - Original Draf. L.W. validation, Formal analysis, Resources, and Writing - Review & Editing. W.H. formal analysis, Visualization and Data Curation. T.Y. validation, Supervision, and Writing - Review & Editing.

Received: July 11, 2022; Revised: August 16, 2022; Accepted: August 16, 2022

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.


Sepsis-associated myocardial injury, an invertible myocardial depression, is a common complication of sepsis. Neogambogic acid is an active compound in garcinia and exerts anthelmintic, anti-inflammatory, and detoxification properties. The role of neogambogic acid in sepsis-associated myocardial injury was assessed. Firstly, mice were pretreated with neogambogic acid and then subjected to lipopolysaccharide treatment to induce sepsis. Results showed that lipopolysaccharide treatment induced up-regulation of biomarkers involved in cardiac injury, including lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), and troponin I (cTnI). However, pretreatment with neogambogic acid reduced levels of LDH, CK-MB, and cTnI, and ameliorated histopathological changes in the heart tissues of septic mice. Secondly, neogambogic acid also improved cardiac function in septic mice through reduction in left ventricular end-diastolic pressure, and enhancement of ejection fraction, fractional shortening, and left ventricular systolic mean pressure. Moreover, neogambogic acid suppressed cardiac apoptosis and inflammation in septic mice and reduced cardiac fibrosis. Lastly, protein expression of p-p38, p-JNK, and p-NF-κB in septic mice was decreased by neogambogic acid. In conclusion, neogambogic acid exerted anti-apoptotic, anti-fibrotic, and anti-inflammatory effects in septic mice through the inactivation of MAPK/NF-κB pathway.

Keywords: Apoptosis, Fibrosis, Myocardial reperfusion, Neo-gambogic acid, p38 MAPK, Sepsis