Brief Article
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World J Gastroenterol. Jan 14, 2013; 19(2): 241-248
Published online Jan 14, 2013. doi: 10.3748/wjg.v19.i2.241
Atorvastatin and rosuvastatin do not prevent thioacetamide induced liver cirrhosis in rats
Haim Shirin, Efrat Sharvit, Hussein Aeed, Dov Gavish, Rafael Bruck
Haim Shirin, Gastroenterology Institute, Assaf Harofeh Medical Center, Zerifin 70300, Israel
Hussein Aeed, Department of Gastroenterology, The E. Wolfson Medical Center, Holon 58100, Israel
Dov Gavish, Department of Internal Medicine “A”, The E. Wolfson Medical Center, Holon 58100, Israel
Rafael Bruck, Efrat Sharvit, Department of Gastroenterology, Tel Aviv Sourasky Medical Center, Tel Aviv 64239, Israel
Haim Shirin, Dov Gavish, Rafael Bruck, Sackler School of Medicine Tel-Aviv University, Tel-Aviv 69975, Israel
Author contributions: Aeed H performed the majority of the in vivo experiments; Sharvit E performed the majority of the in vitro experiments; Gavish D was involved in designing and editing the manuscript; Shirin H and Bruck R designed the study and wrote the manuscript.
Correspondence to: Haim Shirin, MD, Gastroenterology Institute, Assaf Harofeh Medical Center, Zerifin 70300, Israel. haimsh@asaf.health.gov.il
Telephone: +972-8-9779722 Fax: +972-8-9542047
Received: March 25, 2012
Revised: August 31, 2012
Accepted: September 19, 2012
Published online: January 14, 2013
Abstract

AIM: To examine whether the administration of atorvastatin and rosuvastatin would prevent experimentally-induced hepatic cirrhosis in rats.

METHODS: Liver cirrhosis was induced by injections of thioacetamide (TAA). Rats were treated concurrently with TAA alone or TAA and either atorvastatin (1,10 and 20 mg/kg) or rosuvastatin (1, 2.5, 5, 10 and 20 mg/kg) given daily by nasogastric gavage.

RESULTS: Liver fibrosis and hepatic hydroxyproline content, in the TAA-treated group was significantly higher than those of the controls [11.5 ± 3.2 vs 2.6 ± 0.6 mg/g protein (P = 0.02)]. There were no differences in serum aminotransferase levels in the TAA controls compared to all the groups treated concomitantly by statins. Both statins used in our study did not prevent liver fibrosis or reduce portal hypertension, and had no effect on hepatic oxidative stress. Accordingly, the hepatic level of malondialdehyde was not lower in those groups treated by TAA + statins compared to TAA only. In vitro studies, using the BrdU method have shown that atorvastatin had no effect of hepatic stellate cells proliferation. Nevertheless, statin treatment was not associated with worsening of liver damage, portal hypertension or survival rate.

CONCLUSION: Atorvastatin or rosuvastatin did not inhibit TAA-induced liver cirrhosis or oxidative stress in rats. Whether statins may have therapeutic applications in hepatic fibrosis due to other etiologies deserve further investigation.

Keywords: Liver cirrhosis, Statins, Thioacetamide