Khoshakhlagh Mahdieh, Butler Alexandra E, Jamialahmadi Tannaz, Sahebkar Amirhossein
Department of Medical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Research Department, Royal College of Surgeons in Ireland-Bahrain, PO Box 15503, Adliya, Bahrain.
Curr Med Chem. 2025;32(9):1702-1717. doi: 10.2174/0929867331666230815113921.
Alcoholism is a global health concern. Due to its role as the principal site of ethanol metabolism, the liver endures the most significant amount of tissue damage from heavy drinking. Numerous liver lesions can result from chronic and heavy alcohol use, including steatosis, hepatitis, and fibrosis/cirrhosis. Fatty liver is caused by a redox shift from the oxidized to the reduced form of nicotinamide adenine dinucleotide (NAD+) caused by the ethanol oxidation reaction. The other molecular mechanisms related to the progression of alcohol-induced liver injury are increasing sterol regulatory element-binding protein-1 (SREBP-1) and decreasing PPAR-α activity, cell signaling pathway impairment, reactive oxygen species (ROS) accumulation, and lipid peroxidation. L. rhizomes contain a substance called curcumin, which is naturally yellow in color and is also known as turmeric yellow. Curcumin has powerful biological and pharmacological properties, including antioxidant, anti-inflammatory, antifungal, antibacterial, antitumor, and anticancer effects. It's been employed as a hepatoprotective substance. Current studies have demonstrated the ability of curcumin to prevent the activation of NF-αB in Kupffer cells endotoxins, to suppress the expression of various cytokines, chemokines, cyclooxygenase-2 (COX-2), and iNOS, as well as to modulate immune responses. The present study has shown the vital role of curcumin in a variety of hepatotoxic procedures, and summarizes those effects, focusing on the molecular insights they provide.
酒精中毒是一个全球性的健康问题。由于肝脏是乙醇代谢的主要场所，大量饮酒对肝脏造成的组织损伤最为严重。长期大量饮酒会导致多种肝脏病变，包括脂肪变性、肝炎以及纤维化/肝硬化。脂肪肝是由乙醇氧化反应导致烟酰胺腺嘌呤二核苷酸（NAD+）从氧化形式向还原形式的氧化还原转变引起的。与酒精性肝损伤进展相关的其他分子机制包括固醇调节元件结合蛋白-1（SREBP-1）增加、过氧化物酶体增殖物激活受体-α（PPAR-α）活性降低、细胞信号通路受损、活性氧（ROS）积累以及脂质过氧化。姜黄根茎含有一种名为姜黄素的物质，其天然呈黄色，也被称为姜黄烯。姜黄素具有强大的生物学和药理特性，包括抗氧化、抗炎、抗真菌、抗菌、抗肿瘤和抗癌作用。它已被用作一种肝脏保护物质。目前的研究表明，姜黄素能够阻止库普弗细胞中NF-αB因内毒素而激活，抑制各种细胞因子、趋化因子、环氧化酶-2（COX-2）和诱导型一氧化氮合酶（iNOS）的表达，并调节免疫反应。本研究显示了姜黄素在多种肝毒性过程中的重要作用，并总结了这些作用，重点关注它们所提供的分子见解。
