Curcumin in Liver Diseases: A Systematic Review of the Cellular Mechanisms of Oxidative Stress and Clinical Perspective

Abstract

Oxidative stress has been considered a key causing factor of liver damage induced by a variety of agents, including alcohol, drugs, viral infections, environmental pollutants and dietary components, which in turn results in progression of liver injury, non-alcoholic steatohepatitis, non-alcoholic liver disease, liver fibrosis and cirrhosis. During the past 30 years and even after the major progress in the liver disease management, millions of people worldwide still suffer from an acute or chronic liver condition. Curcumin is one of the most commonly used indigenous molecules endowed by various shielding functionalities that protects the liver. The aim of the present study is to comprehensively review pharmacological effects and molecular mechanisms, as well as clinical evidence, of curcumin as a lead compound in the prevention and treatment of oxidative associated liver diseases. For this purpose, electronic databases including “Scopus,” “PubMed,” “Science Direct” and “Cochrane library” were extensively searched with the keywords “curcumin or curcuminoids” and “hepatoprotective or hepatotoxicity or liver” along with “oxidative or oxidant.” Results showed that curcumin exerts remarkable protective and therapeutic effects of oxidative associated liver diseases through various cellular and molecular mechanisms. Those mechanisms include suppressing the proinflammatory cytokines, lipid perodixation products, PI3K/Akt and hepatic stellate cells activation, as well as ameliorating cellular responses to oxidative stress such as the expression of Nrf2, SOD, CAT, GSH, GPx and GR. Taking together, curcumin itself acts as a free radical scavenger over the activity of different kinds of ROS via its phenolic, β-diketone and methoxy group. Further clinical studies are still needed in order to recognize the structure-activity relationships and molecular mechanisms of curcumin in oxidative associated liver diseases.

Does turmeric/curcumin supplementation improve serum alanine aminotransferase and aspartate aminotransferase levels in patients with nonalcoholic fatty liver disease? A systematic review and meta‐analysis of randomized controlled trials

“…Another possible mechanism in this regard is that turmeric/curcumin can improve insulin resistance as a key factor for NAFLD pathogenesis (Tabrizi et al, 2018). In addition, they might ameliorate fatty liver disease progression through inhibiting fatty acids synthesis and biosynthesis of unsaturated fatty acids, such as stearic acid, linoleic acid, and oleic acid (Egashira, Sasaki, Higuchi, & Ieiri, 2012;Farzaei et al, 2018).…”

Current Biomedical Use of Copper Chelation Therapy

“…In recent years, other compounds have been tested in animal models. Among them, DMP-1001 {methyl 4-[7-hydroxy-10,13-dimethyl-3-({4-[(pyridin-2-ylmethyl)amino]butyl}amino)hexadecahydro-1H-cyclopenta [a]phenanthren-17-yl]pentanoate} [43]; methanobactin [44], trientine delivered through liposomes [45] and curcumin [46]. These drugs, however, need further studies both in vitro and in vivo as they have not been used in clinical trials so far.…”

Carbon Monoxide Being Hydrogen Sulfide and Nitric Oxide Molecular Sibling, as Endogenous and Exogenous Modulator of Oxidative Stress and Antioxidative Mechanisms in the Digestive System

“…Therefore, this organ remains at the high risk of oxidative injury caused by the production of ROS. Oxidative stress has been considered a key factor causing liver damage induced by a variety of chemical and nonchemical agents, including alcohol, drugs, hepatic viral infections, and nutritional components, which in turn causes progression of hepatic injury, liver fibrosis, cirrhosis, and in some cases hepatocellular carcinoma [78][79][80][81]. These highly reactive species can be responsible for hepatic I/R injury occurring during surgical procedures such as liver resection and liver transplantation [82,83].…”