Reports of Biochemistry
and Molecular Biology
Wed, Dec 24, 2025
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Vol.14 No.2 Jul
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Department of Toxicology, Faculty of Pharmacy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran & Toxicology Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Abstract: (28 Views)
Background: Arsenic is a serious threat to human health. Long-term exposure to arsenic has been linked to various harmful health effects, including liver damage. The liver damage caused by arsenic is mainly due to inflammation and oxidative stress. This research was performed to investigate the hepatoprotective effects of herniarin (HER), a coumarin derivative found in many plants, against hepatotoxicity induced by sodium arsenite (SA).
Methods: To induce hepatotoxicity, SA at a dose of 10 mg/kg was administered to mice for 30 days. HER at doses of 10, 25, and 50 mg/kg was given to mice for 30 days before SA administration. After completing the study protocol, the animals were euthanized, and blood and liver samples were collected for biochemical assessments.
Results: The results showed that SA increased liver enzymes and causes tissue damage, as well as elevated oxidative substances such as substances reactive to thiobarbituric acid in the liver, while simultaneously leading to a decrease in total thiol reserves and decreases in antioxidant enzymes such as catalase, superoxide dismutase, and glutathione peroxidase. Western blot analysis showed decreased protein expression of Nrf2, NQO1, and HO-1.
Conclusions: Pretreatment with HER ameliorated SA-associated liver injury in mice. HER reduced hepatotoxicity and oxidative damage caused by SA and increased antioxidant factors.
Methods: To induce hepatotoxicity, SA at a dose of 10 mg/kg was administered to mice for 30 days. HER at doses of 10, 25, and 50 mg/kg was given to mice for 30 days before SA administration. After completing the study protocol, the animals were euthanized, and blood and liver samples were collected for biochemical assessments.
Results: The results showed that SA increased liver enzymes and causes tissue damage, as well as elevated oxidative substances such as substances reactive to thiobarbituric acid in the liver, while simultaneously leading to a decrease in total thiol reserves and decreases in antioxidant enzymes such as catalase, superoxide dismutase, and glutathione peroxidase. Western blot analysis showed decreased protein expression of Nrf2, NQO1, and HO-1.
Conclusions: Pretreatment with HER ameliorated SA-associated liver injury in mice. HER reduced hepatotoxicity and oxidative damage caused by SA and increased antioxidant factors.
Type of Article: Original Article |
Subject:
Biochemistry
Received: 2025/05/11 | Accepted: 2025/11/10
Received: 2025/05/11 | Accepted: 2025/11/10
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