Hormetic effects of curcumin on oxidative stress injury induced by trivalent arsenic in isolated rat hepatocytes.

IF 2.2 Q3 CHEMISTRY, MEDICINAL Avicenna Journal of Phytomedicine Pub Date : 2023-11-01 DOI:10.22038/AJP.2023.22634

Marzieh Amirmostofian, Fahimeh Akbari, Mahmoud Hashemzaei, Fahimeh Safaeinejad, Kaveh Tabrizian, Halimeh Arbab, Ramin Rezaee, Shaghayegh Hemat Jouy, Vahideh Ghorani, Jafar Shahraki

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Abstract

Objective: Arsenic (As) poisoning is a worldwide public health problem. Arsenic can cause cancer, diabetes, hepatic problems, etc. Hence, we investigated possible hepatoprotective properties of curcumin against As³⁺-induced liver damages in freshly isolated rat hepatocytes.

Materials and methods: Isolation of hepatocytes was done by the two-step liver perfusion method using collagenase. The EC₅₀ concentration of As³⁺ was used in toxicity assessments and curcumin (2, 5, and 10 µM) was added 15 min before As³⁺ addition to isolated hepatocytes. Curcumin impact was assessed in terms of cytotoxicity, lipid peroxidation induction, reactive oxygen species (ROS) levels, and mitochondrial membrane potential.

Results: As³⁺ significantly increased cytotoxicity, malondialdehyde and ROS levels and induced mitochondrial membrane damage and hepatocyte membrane lysis after 3 hr incubation. Curcumin 2 µM significantly prevented lipid peroxidation induction, ROS formation, and mitochondrial membrane damage; while curcumin 5 µM had no apparent effect on these parameters, curcumin 10 µM potentiated them.

Conclusion: Curcumin only at low doses could ameliorate oxidative stress injury induced by As³⁺ in isolated rat hepatocytes.

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姜黄素对三价砷诱导的离体大鼠肝细胞氧化应激损伤的激素效应

目的：砷（As）中毒是一个世界性的公共卫生问题。砷可导致癌症、糖尿病、肝脏问题等。因此，我们研究了姜黄素对新鲜分离的大鼠肝细胞中 As3+ 诱导的肝损伤可能具有的保肝特性：采用胶原酶两步肝脏灌流法分离肝细胞。在毒性评估中使用 As3+ 的 EC50 浓度，并在向离体肝细胞添加 As3+ 前 15 分钟添加姜黄素（2、5 和 10 µM）。姜黄素对细胞毒性、脂质过氧化诱导、活性氧（ROS）水平和线粒体膜电位的影响进行了评估：结果：培养 3 小时后，As3+ 会明显增加细胞毒性、丙二醛和 ROS 水平，并诱导线粒体膜损伤和肝细胞膜裂解。姜黄素 2 µM 可明显防止脂质过氧化诱导、ROS 形成和线粒体膜损伤；姜黄素 5 µM 对这些参数无明显影响，而姜黄素 10 µM 则会增强这些参数：结论：只有小剂量姜黄素才能减轻 As3+ 对离体大鼠肝细胞造成的氧化应激损伤。

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