Why Should Prednisolone Suppress Hepatic Ischemia-Reperfusion Injury?

Main Category: Liver Disease / Hepatitis
Also Included In: Transplants / Organ Donations;  GastroIntestinal / Gastroenterology
Article Date: 08 Oct 2008 - 10:00 PDT

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Hepatic ischemia-reperfusion injury is a serious complication but unavoidable problem in liver surgery including liver transplantation and hepatic resection. The most important consequence of this pathological process is multiple organ failure with a high mortality rate. Steroid therapy suppresses liver injury by a variety of mechanisms, including increased tissue blood flow and suppression of oxygen free radicals, arachidonic acid derivatives, lysosomal proteases (cathepsins) and cytokine production. However, the exact intracellular mechanisms of steroid action on hepatic ischemia-reperfusion injury remains unknown.

A research article published in the World Journal of Gastroenterology addresses this question. This research team was led by Prof. Meng Wang from Eastern Hepatobiliary Surgery Hospital of Shanghai.

The hepatic ischemia-reperfusion injury model was performed through clamped the left lateral and median lobes of rat liver (68%) for 60 minutes and followed by 120 minutes reperfusion. Prednisolone was administered at 1.0, 3.0, or 10 mg/kg at 30 min before ischemia. In addition to biochemical and microscopic analyses, activation of calpain mu was determined using specific antibodies against the intermediate (activated) form of calpain. Degradation of talin was also studied by Western blotting.

They found that in the control and prednisolone (1.0 mg/kg) groups, serum aspartate transaminase (AST) and alanine transaminase (ALT) level were elevated, and cell membrane bleb formation was observed after 120 min of reperfusion. Moreover, calpain mu activation and talin degradation were detected. Infusion of prednisolone at 3.0 or 10 mg/kg significantly suppressed serum AST and ALT, and prevented cell membrane bleb formation. At 10 mg/kg, prednisolone markedly suppressed calpain mu activation and talin degradation.

Their results indicate that prednisolone can suppress ischemia-reperfusion injury of the rat liver. Its cytoprotective effect is closely associated with the suppression of calpain mu activation and talin degradation.

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Article adapted by Medical News Today from original press release.
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Reference: Wang M, Shen F, Shi LH, Xi T, Li XF, Chen X, Wu MC. Protective effect of prednisolone on ischemia-induced liver injury rats. World J Gastroenterol 2008;14(27):4332-4337 http://www.wjgnet.com/1007-9327/14/4332.asp

Correspondence to: Meng Wang, MD, Ph.D, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, 225, Changhai Road, Shanghai 200438, 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.

About The WJG Press

The WJG Press mainly publishes World Journal of Gastroenterology.

Source: Lai-Fu Li
World Journal of Gastroenterology