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Deoxyelephantopin—a novel PPARγ agonist regresses pressure overload-induced cardiac fibrosis via IL-6/STAT-3 pathway in crosstalk with PKCδ by Anirban Banik; Ratul Datta Chaudhuri; Shubham Vashishtha; Soumyadeep Gupta; Abhik Kar; Abhijit Bandyopadhyay; Bishwajit Kundu; Sagartirtha Sarkar is a Neuroscience article available to read on EtoBox.

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Pathological cardiac hypertrophy is associated with ventricular fibrosis leading to heart failure. The use of thiazolidinediones as Peroxisome Proliferator-Activated Receptor-gamma (PPARγ)-modulating anti-hypertrophic therapeutics has been restricted due to major side-effects. The present study aims to evaluate the anti-fibrotic potential of a novel PPARγ agonist, deoxyelephantopin (DEP) in cardiac hypertrophy. AngiotensinII treatment in vitro and renal artery ligation in vivo were performed to mimic pressure overload-induced cardiac hypertrophy. Myocardial fibrosis was evaluated by Masson's trichrome staining and hydroxyproline assay. Our results showed that DEP treatment significantly improves the echocardiographic parameters by ameliorating ventricular fibrosis without any bystander damage to other major organs. Following molecular docking, all-atomistic molecular dynamics simulation, reverse transcription-polymerase chain reaction and immunoblot analyses, we established DEP as a PPARγ agonist stably interacting with the ligand-binding domain of PPARγ. DEP specifically downregulated the Signal Transducer and Activator of Transcription (STAT)-3-mediated collagen gene expression i

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Author

Anirban Banik; Ratul Datta Chaudhuri; Shubham Vashishtha; Soumyadeep Gupta; Abhik Kar; Abhijit Bandyopadhyay; Bishwajit Kundu; Sagartirtha Sarkar

Publisher

Elsevier BV

Published

2023

Language

EN

Field

Neuroscience (Life Sciences)