Abstract

In aquatic animals, hydrogen peroxide (H2O2), which is a source of oxidative stress, can cause physiological dysfunction, inflammation, and death. Sanguinarine (SAN) is a plant extract known to improve antioxidant and immune capacity. However, the roles of SAN in H2O2-induced liver tissue toxicity is unclear. The effects on hepatic oxidative damage, inflammatory response, and apoptosis were investigated by feeding rice field eel with 0, 375, and 750 μg/kg of SAN for eight weeks and then intraperitoneally injected with H2O2. The results showed that after 24 h of H2O2 injection, the activities of ALT and AST in serum were significantly increased, oxidative damage and inflammatory response occurred in the liver, and apoptosis was induced, which indicated that H2O2 induced liver damage in rice field eel. However, dietary supplemented with 375 or 750 μg/kg SAN significantly decreased the activities of ALT and AST in serum, and significantly increased the antioxidant function (decreased ROS, MDA, and antioxidant enzymes levels, downregulated antioxidant-related gene expression, and inhibited the transcription level of nrf2). The addition of SAN at 375 or 750 μg/kg ameliorated H2O2-induced inflammatory response of liver (upregulated tgf-β1 mRNA expression, downregulated il-1β, il-6, il-8, and il-12β mRNA expression, and inhibited the transcription levels of tlr-3 tlr-7, and nf-κb). In addition, dietary supplemented with 375 or 750 μg/kg SAN alleviated the apoptosis of liver induced by H2O2 (downregulated bax mRNA expression, upregulated caspase3 mRNA expression, and reduced the number of apoptotic cells by TUNEL staining). Overall, these results suggested that SAN could alleviate the liver injury in rice field eel induced by H2O2, mainly by improving antioxidant capacity, alleviating inflammatory response and inhibiting apoptosis, and the effect of 750 μg/kg SAN addition is better than 375 μg/kg.

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