PMID: 15244070Jul 13, 2004Paper

Pitavastatin enhances the anti-fibrogenesis effects of candesartan, an angiotensin II receptor blocker, on CCl4-induced liver fibrosis in rats

Journal of UOEH
Lianbo NieHikaru Ueno

Abstract

It has been shown that a statin (3-hydroxy-3-methyl-glutaryl coenzyme reductase inhibitor) enhances a suppressive effect of angiotensin II type 1 receptor (AT1-R) blocker (ARB) on injury-induced transforming growth factor (TGF)-beta expression in kidneys. We have shown that TGF-beta plays a crucial role in the development of liver fibrosis. In this study, we tested whether a combinatory use of a statin (pitavastatin) and an ARB (candesartan) may further inhibit liver fibrogenesis in carbon tetrachloride (CCl4)-treated rats. Candesartan (8 mg/kg/day) significantly suppressed injury-induced TGF-beta 1 expression in livers, and attenuated fibrogenesis, as evaluated by masson-trichrome staining and hydroxyproline content in livers. Pitavastatin (2 mg/kg/day) alone did not affect liver fibrogenesis. However, it enhanced significantly the suppressive effects of candesartan on TGF-beta 1 expression and fibrogenesis. Although we do not know the underlying molecular mechanisms at this moment, these results suggest that a combinatory use of a statin and an ARB may confer beneficial effects on human liver fibrogenesis.

Citations

Dec 6, 2008·American Journal of Physiology. Gastrointestinal and Liver Physiology·Montserrat MorenoRamón Bataller
Jul 29, 2017·Current Gastroenterology Reports·Jose Ignacio VargasJuan Pablo Arab
Jun 15, 2017·PloS One·Johanneke J AkershoekMagda M W Ulrich
Mar 24, 2016·Gastroenterology Research and Practice·Newaz HossainSmruti R Mohanty

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