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Abstract Title:

Neferine attenuates doxorubicin-induced fibrosis and hypertrophy in H9c2 cells.

Abstract Source:

J Biochem Mol Toxicol. 2022 Mar 28:e23054. Epub 2022 Mar 28. PMID: 35347819

Abstract Author(s):

Bharathi Priya Lohanathan, Baskaran Rathinasamy, Chih-Yang Huang, Vijaya Padma Viswanadha

Article Affiliation:

Bharathi Priya Lohanathan

Abstract:

Doxorubicin (DOX), an anthracycline antineoplastic candidate is used to treat various malignancies. Around 41% of patients undergoing DOX treatment develop acute cardiotoxicity. Preventing DOX-induced cardiac fibrosis and hypertrophy helps in evading cardiac remodeling leading to cardiomyopathy and heart failure. Neferine, an alkaloid from the lotus has numerous pharmacological activities. The present study was designed to evaluate the protective effect of neferine on DOX-mediated fibrosis and hypertrophy. DOX-induced fibrosis involves activation of transforming growth factor-β1 (TGF-β1), matrix metalloproteinase 2 (MMP-2), and MMP-9 with concomitant downregulation of tissue inhibitors of MMPs (TIMP)-1 and TIMP-2 expressions in H9c2 cardiomyoblasts. Furthermore, DOX treatment also resulted in hypertrophy with the increased cell volume and overexpression of hypertrophymarkers calcineurin, brain natriuretic peptide, and atrial natriuretic peptide. Finally, DOX treatment resulted in apoptosis through activation of p53. Pretreatment with neferine markedly activated SIRT1 expression and modulated the expression levels of TGF-β1 and p53, thereby significantly reducing DOX-induced fibrosis, hypertrophy, and apoptosis in H9c2 cardiomyoblasts.

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