Abstract
• Saponified astaxanthin (Asta) extract showed increased in vitro antioxidant activity. • Asta pre-treatment alleviated Paracetamol induced oxidative stress. • Asta pre-treatment decreased GST-P foci, p53, and p38 expressions in rat liver. • Non-saponification Asta pre-treatment stimulated Hemoxygenase-1 expression. • Saponification Asta pre-treatment increased NAD(P)H: quinine oxidoreductase-1 level. Astaxanthin (Asta) extracts from Penaeus sinensis by-products showed increased in vitro antioxidant activity after saponification as compared to the non-saponification Asta. The increases of geometrical Asta (activity order of 9-cis > 13-cis > all- trans ) and Asta stereoisomers could be responsible for the improved antioxidant activities of saponification Asta. Non-saponification or saponification Asta (150 mg/kg) was administered in Sprague-Dawley rats via gavage daily for 14 days before paracetamol (PCM)-induced (400 mg/kg) acute hepatotoxicity. Pre-treatment with non-saponification or saponification Asta counterbalanced rats liver oxidative stress by PCM-induction through restoring reduced glutathione content, total superoxide dismutase and glutathione peroxidase activities. Moreover, Asta pre-treatment decreased glutathione-S-transferase-P (placental form ) foci, p53 and p38 expressions as compared to the model group. Pre-treated with Asta up-modulated phase-II enzyme NAD(P)H: quinine oxidoreductase-1 or Hemoxygenase-1 expressions, indicating the nuclear erythroid 2-related factor 2-antioxidant response element (Nrf2-ARE) pathway for the non-saponification or saponification Asta to alleviate PCM-induced hepatotoxicity in rats.
Published Version
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