Ameliorative Effect of Biochanin A against Gentamicin-induced Nephrotoxicity in Rats

ABSTRACT

Background: Gentamicin (GM), a commonly used aminoglycoside anti-biotic, is effective against various bacterial infections. However, its clinical use is often limited due to its significant nephrotoxic side effects. Nephrotoxicity results from oxidative stress, inflammation, and apoptosis of renal cells. In previous research, Biochanin A (BCA), a natural isoflavone found in various plants, has demonstrated antioxidant, anti-inflammatory, and anti-apoptotic properties. This study explores the potential protective effects of BCA against GM-induced nephrotoxicity. Objectives: To investigate the protective effects of BCA on GM-induced nephrotoxicity in male Wistar rats by assessing kidney function, oxidative stress markers, inflammatory response, and apoptotic regulation. Materials and Methods: Male Wistar rats were divided into four groups, each group containing six animals: Group 1 as the control, Group 2 received BCA alone [50 mg/kg, intraperitoneal (IP)], Group 3 received GM alone (100 mg/kg, IP), and Group 4 received BCA (50 mg/kg, IP) along with GM (100 mg/kg, IP). At the end of the experiment day (on the 12th day), the animals were sacrificed, the organs were removed, and used for the following parameters. Results: GM administration significantly increased the levels of creatinine, urea, uric acid, blood urea nitrogen (BUN), and lipid peroxidation levels and decreased the levels of antioxidant enzymes. Administration with BCA has significantly mitigated kidney function markers and oxidative stress while enhancing antioxidant activities. Furthermore, GM-induced rats exhibited significant upregulation in proinflammatory cytokines, proapoptotic proteins, and downregulation of anti-apoptotic proteins. Administration of BCA significantly downregulated proinflammatory cytokines and proapoptotic proteins and upregulated anti-apoptotic proteins in GM-induced rats. These results underscore the utility of necrotic and apoptotic markers in the early detection of tubular kidney damage. Conclusion: This study conclusively demonstrates that BCA protects the kidneys from GM-induced oxidative stress, inflammation, and apoptosis of renal tubular cells, offering promise for mitigating GM-induced nephrotoxicity.

KEYWORDS

• Nephrotoxicity
• Biochanin A
• gentamycin
• oxidative stress
• apoptosis

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• DOI10.1177/09731296251313612Copy

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