Protective Effects of Curcumin against Alcoholic Fatty Liver

姜黄素 化学 药理学 生物化学 酒精性脂肪肝 脂肪肝 医学 内科学 疾病
作者
Mahdieh Khoshakhlagh,Alexandra E. Butler,Tannaz Jamialahmadi,Amirhossein Sahebkar
出处
期刊:Current Medicinal Chemistry [Bentham Science Publishers]
卷期号:32 (9): 1702-1717 被引量:8
标识
DOI:10.2174/0929867331666230815113921
摘要

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. Curcuma longa 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 via 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.
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