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Hepatoprotective Effect of Meroterpenoid-Rich Fraction from the Ethanolic Extract of Sargassum sarratifolium on tert -Butyl Hydroperoxide-Induced Mice

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The liver, critical for detoxification and metabolic homeostasis, is highly susceptible to oxidative stress caused by reactive oxygen species (ROS). This study evaluated the hepatoprotective effects of a meroterpenoid-rich fraction (MES) from Sargassum serratifolium in a tert-butyl hydroperoxide (tBHP)-induced oxidative liver injury model in mice. MES treatment ameliorated t-BHP-induced histopathological changes, including hepatocyte swelling, cytoplasmic vacuolation, and necrosis. Biochemical analyses showed that MES significantly decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities to 70% and 50%, respectively, of the levels observed in the t-BHP-treated group. It also reduced Lactate Dehydrogenase (LDH) activity, which was increased fivefold by t-BHP, by up to 70%, and significantly reduced hepatic Malondialdehyde (MDA) levels. MES restored the activities of antioxidant enzymes including Superoxide Dismutase (SOD), catalase, Glutathione Peroxidase (GPx), and Glutathione Reductase (GR), and activated the Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) pathway, leading to increased glutathione (GSH) levels and enhancing the expression of detoxifying enzymes such as heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase 1 (NQO1). These findings demonstrate that MES provides effective protection against oxidative liver damage by mitigating oxidative stress, enhancing antioxidant defenses, and activating the Nrf2 signaling pathway. This highlights the potential of marine-derived natural products as hepatoprotective agents.

Abstract

The liver, critical for detoxification and metabolic homeostasis, is highly susceptible to oxidative stress caused by reactive oxygen species (ROS). This study evaluated the hepatoprotective effects of a meroterpenoid-rich fraction (MES) from Sargassum serratifolium in a tert-butyl hydroperoxide (tBHP)-induced oxidative liver injury model in mice. MES treatment ameliorated t-BHP-induced histopathological changes, including hepatocyte swelling, cytoplasmic vacuolation, and necrosis. Biochemical analyses showed that MES significantly decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities to 70% and 50%, respectively, of the levels observed in the t-BHP-treated group. It also reduced Lactate Dehydrogenase (LDH) activity, which was increased fivefold by t-BHP, by up to 70%, and significantly reduced hepatic Malondialdehyde (MDA) levels. MES restored the activities of antioxidant enzymes including Superoxide Dismutase (SOD), catalase, Glutathione Peroxidase (GPx), and Glutathione Reductase (GR), and activated the Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) pathway, leading to increased glutathione (GSH) levels and enhancing the expression of detoxifying enzymes such as heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase 1 (NQO1). These findings demonstrate that MES provides effective protection against oxidative liver damage by mitigating oxidative stress, enhancing antioxidant defenses, and activating the Nrf2 signaling pathway. This highlights the potential of marine-derived natural products as hepatoprotective agents.

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