Hepatoprotective potential of vanillic acid against isoniazid-rifampicin-induced liver toxicity

Liver toxicity induced by antitubercular drugs, such as isoniazid and rifampicin, poses a significant clinical challenge due to oxidative stress and hepatocellular damage. This study evaluated the hepatoprotective potential of vanillic acid in mitigating drug-induced liver injury in rats. Hepatotoxicity was induced by administering isoniazid and rifampicin, followed by treatment with vanillic acid at two different doses (50 mg/kg and 100 mg/kg). Silymarin, a well-known hepatoprotective agent, was used as a reference standard. Biochemical markers, including aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), superoxide dismutase (SOD), catalase, and bilirubin, were assessed to evaluate liver function and oxidative stress. Results revealed significant elevation in AST, ALT, ALP, and bilirubin levels and a reduction in antioxidant enzymes (SOD and catalase) in the isoniazid and rifampicin-treated group, indicating severe liver damage. Co-administration of vanillic acid significantly reduced these elevated markers and restored antioxidant enzyme levels in a dose-dependent manner. The higher dose of vanillic acid (100 mg/kg) exhibited a more pronounced hepatoprotective effect, comparable to silymarin. These findings suggest that vanillic acid exerts its protective effects by enhancing antioxidant defense, reducing oxidative stress, and preserving liver cell integrity. This study highlights the therapeutic potential of vanillic acid in preventing drug-induced liver toxicity and underscores its role as a promising candidate for hepatoprotection during antitubercular therapy. Further investigation into its molecular mechanisms and clinical applicability is warranted. • Vanillic acid significantly reduces liver damage caused by hepatotoxic drugs. • Improved antioxidant enzyme activity demonstrates vanillic acid's protective effects. • Liver enzyme leakage and bilirubin accumulation are effectively minimized. • Dose-dependent restoration of liver function suggests vanillic acid's efficacy. • Vanillic acid shows promise as a therapeutic agent for hepatoprotection.

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Publication Details

Journal
Aspects of Molecular Medicine
Published
2025-04-25
DOI
https://doi.org/10.1016/j.amolm.2025.100087
Citations
3
Primary Topic
Drug-Induced Hepatotoxicity and Protection
Type
article
Field-Weighted Citation Impact
3.11
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article

Hepatoprotective potential of vanillic acid against isoniazid-rifampicin-induced liver toxicity

Aditya Ganeshpurkar, Nazneen Dubey, Mohammad Hassan Khadem Ansari
3 citations
Aspects of Molecular Medicine
Drug-Induced Hepatotoxicity and Protection
3.11
article

Hepatoprotective potential of vanillic acid against isoniazid-rifampicin-induced liver toxicity

Aditya Ganeshpurkar, Nazneen Dubey, Mohammad Hassan Khadem Ansari
article en
3 citations

Abstract

Liver toxicity induced by antitubercular drugs, such as isoniazid and rifampicin, poses a significant clinical challenge due to oxidative stress and hepatocellular damage. This study evaluated the hepatoprotective potential of vanillic acid in mitigating drug-induced liver injury in rats. Hepatotoxicity was induced by administering isoniazid and rifampicin, followed by treatment with vanillic acid at two different doses (50 mg/kg and 100 mg/kg). Silymarin, a well-known hepatoprotective agent, was used as a reference standard. Biochemical markers, including aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), superoxide dismutase (SOD), catalase, and bilirubin, were assessed to evaluate liver function and oxidative stress. Results revealed significant elevation in AST, ALT, ALP, and bilirubin levels and a reduction in antioxidant enzymes (SOD and catalase) in the isoniazid and rifampicin-treated group, indicating severe liver damage. Co-administration of vanillic acid significantly reduced these elevated markers and restored antioxidant enzyme levels in a dose-dependent manner. The higher dose of vanillic acid (100 mg/kg) exhibited a more pronounced hepatoprotective effect, comparable to silymarin. These findings suggest that vanillic acid exerts its protective effects by enhancing antioxidant defense, reducing oxidative stress, and preserving liver cell integrity. This study highlights the therapeutic potential of vanillic acid in preventing drug-induced liver toxicity and underscores its role as a promising candidate for hepatoprotection during antitubercular therapy. Further investigation into its molecular mechanisms and clinical applicability is warranted. • Vanillic acid significantly reduces liver damage caused by hepatotoxic drugs. • Improved antioxidant enzyme activity demonstrates vanillic acid's protective effects. • Liver enzyme leakage and bilirubin accumulation are effectively minimized. • Dose-dependent restoration of liver function suggests vanillic acid's efficacy. • Vanillic acid shows promise as a therapeutic agent for hepatoprotection.

Aspects of Molecular MedicineVol. 5
Shriram Institute for Industrial Research (IN)
Openalex Percentile: Top 11%
Drug-Induced Hepatotoxicity and Protection
3.11
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