Alcohol-induced hepatic fibrosis and the relation between Hepcidin and liver fibrosis | ||||
| Records of Pharmaceutical and Biomedical Sciences | ||||
| Volume 8, Issue 1, 2024, Page 37-44 PDF (500.67 K) | ||||
| Document Type: Mini-reviews | ||||
| DOI: 10.21608/rpbs.2024.221578.1239 | ||||
 View on SCiNiTO | ||||
| Authors | ||||
AL-shimaa A. Ali1; Nora M. Aborehab2; Samy M. Saleh3; Eman T. Mehanna   4
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| 1Department of Biochemistry, Faculty of Pharmacy, Suez Canal University, 41522 Ismailia, Egypt; | ||||
| 2Department of Biochemistry, Faculty of Pharmacy, October University for Modern Sciences and arts (MSA), October 6 City, Egypt | ||||
| 3Department of Biochemistry, Faculty of Pharmacy, Suez Canal University, 41522 Ismailia, Egypt | ||||
| 4Department of Biochemistry, Faculty of Pharmacy, Suez Canal University, Ismailia, 41522, Egypt | ||||
| Abstract | ||||
| Alcoholic liver disease (ALD) is a worldwide health problem that may lead to development of fatty liver steatosis, hepatitis and cirrhosis. Alcohol is known to exert a harmful effect on a variety of human tissues. In particular, the liver is the major site of alcohol-induced damage because it is the direct recipient of the blood that contains elevated levels of alcohol, and it is the major organ responsible for alcohol metabolism. The damage caused by ethanol is mainly attributed to its metabolic process that results in production of acetaldehyde and reactive oxygen species (ROS) such as hydrogen peroxide, superoxide and free hydroxyl radical. These metabolites cause depletion of reduced glutathione (GSH), peroxidation of cellular membranes, oxidation of macro-molecules such as proteins and nucleic acids, and eventually lead to progressive injury of hepatocytes. Additionally, ethanol and its metabolic products enhance the production of pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). The enhanced production of those inflammation factors; stimulated partially by oxidative stress; results in cytokine imbalance and immune disorders, leading to further hepatic damage. Thus, agents with anti-inflammatory and anti-oxidative properties might be potential candidates for protection against alcohol-induced liver disease. The metabolic functions of the alcoholic liver are seriously affected. Disorders in iron metabolism are characteristic of ALD. Abnormal levels of iron, ferritin, and transferrin were reported in ALD. Hepcidin, the principle hepatic regulator of the metabolism of iron, is decreased in ALD. | ||||
| Keywords | ||||
| Alcoholic liver disease; fibrosis; alcohol; cirrhosis; hepcidin | ||||
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