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Anti-inflammatory and antioxidant effect of Moringa oleifera against bisphenol-A-induced hepatotoxicity
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Anti-inflammatory and antioxidant effect of Moringa oleifera against bisphenol-A-induced hepatotoxicity
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Journal Article
Anti-inflammatory and antioxidant effect of Moringa oleifera against bisphenol-A-induced hepatotoxicity
2022
Overview
Non-pharmacological exposure or pharmacological drug-induced hepatic injury is the most common cause of hepatotoxicity. This study was conducted to evaluate the effect of Moringa oleifera leaf extract against bisphenol-A (BPA)-induced hepatic toxicity in rats. Rats (n=56) were randomized into 7 groups (8 rats/each). Control groups: rats received olive oil or Moringa oleifera (400mg/kg) orally for 42 days. Hepatotoxicity groups: rats received BPA (50mg/kg BW) orally in a 1-ml olive oil for 42 days. Reversal groups: rats received Moringa oleifera (200 or 400mg/kg) and BPA (50mg/kg BW) for 42 days. Preventive groups: rats received Moringa oleifera (200 or 400mg/kg) for 30 days followed by BPA (50mg/kg BW) for 14 days. At the end of the experiments, blood samples were collected for glucose and liver function assay, while the liver tissue samples were collected and homogenated for measuring the inflammatory/oxidant and antioxidant markers. Rats with BPA-induced hepatotoxicity have significantly increased serum aspartate transaminase (AST), alanine transaminase (ALT), and glucose; liver lysate malondialdehyde (MDA); tumor necrosis factor (TNF-[alpha]); and macrophage migrating inhibitory factor (MIF) but significantly decreased levels of liver lysate reduced glutathione (GSH) and total antioxidant capacity (TAC) levels. The administration of Moringa oleifera (especially 400mg/kg BW) in both reversal and preventive groups ameliorate the toxic effects of BPA in rats, as it decreased the activities of AST, ALT, glucose, MDA, TNF-[alpha], and MIF levels and increased the antioxidant levels of GSH and TAC. Moringa oleifera has hepatoprotective effects against BPA-induced liver damage through the regulation of antioxidants and inflammatory biomarkers.
Publisher
Springer
Subject
