In Liver Cirrhosis Melatonin May Be Served As A Potential Anti-Fibrotic Drug

Main Category: Liver Disease / Hepatitis
Also Included In: Biology / Biochemistry
Article Date: 01 Apr 2009 - 2:00 PDT

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In China, the incidence of liver cirrhosis is still high. Liver cirrhosis results from fibrosis. If treated properly at fibrosis stage, cirrhosis can be prevented. However, no effective antifibrosis drugs are available at present. Several lines of evidences suggest that oxidative stress plays an important role in the etiopathogenesis of hepatic fibrosis. Melatonin can protect cells, tissues, and organs against oxidative damage induced by a variety of free-radical-generating agents and processes.

A research team led by Professor Jian-Ming Xu from the First Affiliated Hospital of Anhui Medical University, China evaluated the possible fibrosuppressant effect of melatonin in rat. Their study was published on March 28, 2009 in the World Journal of Gastroenterology.

In this study, hepatic fibrosis in rats was successfully induced by subcutaneous injection of sterile CCl4 twice weekly for a total of 12 wk. At the beginning of injection of CCl4, melatonin (2.5, 5, 10 mg/kg body weight) was intraperitoneally administered to the rats daily for 12 wk. Hepatic fibrotic changes were evaluated biochemically by measuring tissue hydroxyproline levels and histopathogical examination. The serum activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) were used to evaluate the hepatic injury. Hepatic oxidative stress markers were evaluated by changes in the amount of lipid peroxides, measured as malondialdehyde (MDA) and glutathione peroxidase (GPx) in liver homogenates. Serum hyaluronic acid (HA), laminin (LN), and procollagen 3 N-terminal peptide (P3NP) were determined as serum markers of hepatic fibrogenesis.

Their results suggested that treatment with melatonin (10 mg/kg) could decrease the scores of hepatic fibrosis grading, reduced the contents of HA, LN in serum and Hydroxyproline (HYP) in liver, treatment with melatonin (5,10 mg/kg ) could decrease serum levels of ALT, AST and blocked the increase in MDA in rats with hepatic injury caused by CCl4.

Their result indicated melatonin could ameliorate CCl4-induced hepatic fibrosis in rats. The protective effect of melatonin on hepatic fibrosis may be related to its antioxidant activities. This may provide a basis for further studies on the potentially protective effect of melatonin on liver function in cirrhotic patients

Notes:

Reference: Hong RT, Xu JM, Mei Q. Melatonin ameliorates experimental hepatic fibrosis induced by carbon tetrachloride in rats. World J Gastroenterol 2009; 15(12): 1452-1458 http://www.wjgnet.com/1007-9327/15/1452.asp

Correspondence to: Jian-Ming Xu, Professor, Department of Gastroenterology, The First Affiliated Hospital of Anhui Medical University, Hefei 230022, Anhui Province, China.

About World Journal of Gastroenterology

World Journal of Gastroenterology (WJG), a leading international journal in gastroenterology and hepatology, has established a reputation for publishing first class research on esophageal cancer, gastric cancer, liver cancer, viral hepatitis, colorectal cancer, and H pylori infection and provides a forum for both clinicians and scientists. WJG has been indexed and abstracted in Current Contents/Clinical Medicine, Science Citation Index Expanded (also known as SciSearch) and Journal Citation Reports/Science Edition, Index Medicus, MEDLINE and PubMed, Chemical Abstracts, EMBASE/Excerpta Medica, Abstracts Journals, Nature Clinical Practice Gastroenterology and Hepatology, CAB Abstracts and Global Health. ISI JCR 2003-2000 IF: 3.318, 2.532, 1.445 and 0.993. WJG is a weekly journal published by WJG Press. The publication dates are the 7th, 14th, 21st, and 28th day of every month. WJG is supported by The National Natural Science Foundation of China, No. 30224801 and No. 30424812, and was founded with the name of China National Journal of New Gastroenterology on October 1, 1995, and renamed WJG on January 25, 1998.

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Source: Lai-Fu Li
World Journal of Gastroenterology