Dina Suhail
PhD in Al-Yarmouk University College, Department of Pharmacy, Iraq
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http://doi.org/10.37648/ijrst.v11i03.001
The inadequacy to replace acetaminophen (APAP) with a more effective analgesic continues its use in therapeutic interventions, upholding the risk of hepatotoxicity. Depletion of glutathione reserves by a metabolic intermediate of acetaminophen, N-acetyl-p-benzoquinone imine (NAPQI), is the major reason. The current study presents the combinatorial effect of metformin, a biguanide, in ameliorating the APAP toxicity. HepG2 cells were used for in vitro studies and MTT and LDH leakage assays were used for viability assessment. 10 μM of metformin improved the cell viability and membrane integrity of cells treated with a high antioxidant enzymes and reduced glutathione were significantly increased in cells co-administrated with metformin and acetaminophen
Keywords: metformin; acetaminophen toxicity; liver toxicity; HepG2 cells; necrosis
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