Hepatoprotective effects of astragalin against polystyrene microplastics induced hepatic damage in male albino rats by modulating Nrf-2/Keap-1 pathway

Abstract

The current study was designed to determine the curative potential of astragalin (AST) against polystyrene microplastics (PS-MPs) induced hepatic toxicity in rats. PS-MPs exposure decreased the expression of Nrf-2 and anti-oxidant enzymes, while increasing Keap-1 expression. The activities of glutathione-S-transferase, catalase, glutathione, glutathione peroxidase, superoxide dismutase, glutathione reductase and heme oxygenase-1 were decreased, besides the levels of malondialdehyde and reactive oxygen species were also increased following the exposure of PS-MPs. The intoxication of PS-MPs elevated aspartate aminotransferase, alanine transaminase, alkaline phosphatase levels, as well as cyclooxygenase-2 activity, interleukin-6, interleukin-1 beta, nuclear factor-kappa B and tumor necrosis factor-alpha levels were also escalated. Furthermore, Bcl-2 expression was down-regulated, while Bax and Caspase-3 expressions were upregulated following PS-MPs exposure. Histopathological assessment revealed substantial liver damages in PS-MPs treated rats. However, AST supplementation substantially recovered PS-MPs-induced damages and histological anomalies. Therefore, AST can be used as a curative agent to treat PS-MPs-prompted hepatotoxicity due to its anti-apoptotic, anti-inflammatory and anti-oxidant potentials.

Keywords

• Polystyrene microplastics
• Astragalin
• Hepatotoxicity
• Inflammation
• Apoptosis