Cardioprotective and Hypolipidemic Effects of Methanolic Stem Bark Extract of Vitex doniana against Gentamicin-induced Myocardial Injury and Dyslipidaemia in Wistar Rats
Asian Journal of Biotechnology and Bioresource Technology · pp. 80–90 · Published 27 Jan 2026
10.9734/ajb2t/2026/v12i1280Abstract
Gentamicin, a widely used aminoglycoside antibiotic, is associated with cardiotoxic effects largely mediated by oxidative stress and lipid metabolic disturbances. This study evaluated the cardioprotective potential of methanolic stem bark extract of Vitex doniana (MSEVD) against gentamicin-induced cardiac injury in Wistar rats. Thirty-six female rats were divided into six groups and treated for 12 days with normal saline, gentamicin (100 mg/kg), gentamicin plus graded doses of MSEVD (100, 200, and 400 mg/kg), or gentamicin plus silymarin (75 mg/kg) used as a positive control. Serum lipid profile parameters (TC, TG, HDL-c, LDL-c, VLDL-c) and atherogenic index (AI) were evaluated, alongside histopathological examination of heart tissues. Gentamicin administration significantly increased TC, TG, LDL-c, and AI, while reducing HDL-c, indicating marked dyslipidaemia and elevated cardiovascular risk. Co-administration of MSEVD significantly ameliorated these alterations in a dose-dependent manner, with the 400 mg/kg dose showing near-complete normalization of lipid indices and superior reduction in VLDL-c compared with the reference drug. Histopathological findings corroborated the biochemical results, showing severe myocardial degeneration, necrosis, inflammation, and vascular damage in gentamicin-treated rats, while MSEVD markedly preserved myocardial architecture, particularly at higher doses. These findings demonstrate that methanolic stem bark extract of Vitex doniana exerts significant cardioprotective and hypolipidaemic effects against gentamicin-induced cardiac injury, likely mediated through its antioxidant and anti-inflammatory phytoconstituents, supporting its potential as a natural therapeutic agent in drug-induced cardiotoxicity.
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