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Fas Receptor Activation by Endogenous Opioids Is a New Mechanism for Cardiomyopathy in Cirrhotic Rats Publisher



Abbasi A1 ; Faramarzi N2 ; Khosravi M3, 4 ; Yazarloo F5 ; Abbasi MA6 ; Dehpour AR3, 4 ; Jahanzad I7
Authors
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Authors Affiliations
  1. 1. Department of Pathology, Urmia University of Medical sciences (UMSU), Urmia, Iran
  2. 2. Department of Medicine, Brigham and Women's Hospital, Biomaterials Innovation Research Center, Harvard Medical School, Cambridge, 02139, MA, United States
  3. 3. Department of Pharmacology, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Experimental Medicine Research Center, Tehran University of Medical Sciences, Tehran, Iran
  5. 5. Department of Medical Genetics, Tehran University of Medical Sciences, Tehran, Iran
  6. 6. Department of Internal Medicine, Shahid Beheshti Medical University, Tehran, Iran
  7. 7. Department of Pathology, Tehran University of Medical sciences (TUMS), Tehran, Iran

Source: Journal of Clinical and Experimental Hepatology Published:2017


Abstract

Background Cirrhosis, a common consequence of chronic liver inflammation is associated with various cardiovascular dysfunctions which are called cirrhotic cardiomyopathy (CC). Among the various possible causes of CC, apoptosis is considered to have a pivotal role. Objectives To explore the contribution of endogenous opioids in the apoptosis process in a rat model of CC. Material and methods Four genes were selected to cover both intrinsic and extrinsic pathways of apoptosis. Cardiac samples from 4 groups of rats were evaluated. Two groups were cirrhotic through bile duct ligation (BDL) receiving either naltrexone (BDL-naltrexone) or saline (BDL-saline), two others were normal rats as sham groups receiving either naltrexone (sham-naltrexone) or saline (sham-saline). Expression level of BCL2, Caspase3, Fas and FasL was explored in all groups using reverse transcriptase real-time PCR. Results BDL-saline group showed significant over-expression of BCL2, caspase3 and Fas. BCL2 expression was 1.44 (P < 0.001) and caspasse3 was 1.35 (P < 0.001) times higher than sham–saline group, Fas was also overexpressed 1.3 (P < 0.001) times higher than BDL-naltrexone group and 1.91 (P < 0.001) compared to sham-naltrexone group. Caspase3 expression was 1.35 (P < 0.001) folds higher than sham-naltrexone group. The expression pattern of FasL revealed no statistically significant change among study groups. Conclusion Fas molecule enrollment during CC is a novel finding. Fas molecule is activated during cirrhosis through elevated levels of endogenous opioids. This pathway is one of the leading causes of CC. Our findings also demonstrated the protective role of naltrexone as opioids antagonist on cardiomyocytes in a rat model of CC. © 2016
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