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The anti-inflammatory and anti-fibrotic effects of tadalafil in thioacetamide- induced liver fibrosis in rats.

A new interesting article has been published in Can J Physiol Pharmacol. 2018 Nov 6. doi: 10.1139/cjpp-2018-0338. [Epub ahead of print] and titled:

The anti-inflammatory and anti-fibrotic effects of tadalafil in thioacetamide- induced liver fibrosis in rats.

Authors of this article are:

Mansour HM, Salama AAA, Abdel-Salam RM, Assaf NA, Yassen NN, Zaki HF.

A summary of the article is shown below:

Liver fibrosis is a health concern that leads to organ failure mediated via production of inflammatory cytokines and fibrotic biomarkers. This study aimed to explore the protective effect of tadalafil, a phosphodiestrase-5 inhibitor, against thioacetamide (TAA) – induced liver fibrosis. Fibrosis was induced by administration of TAA (200 mg/kg, i.p.) twice weekly for 6 weeks. Serum transaminases activities, liver inflammatory cytokines, fibrotic biomarkers, and liver histopathology were assessed. TAA induced marked histopathological changes in liver tissues coupled with elevations in serum transaminases activities. Furthermore, hepatic content of nitric oxide and tumor necrosis factor- alpha , interlukin-6 and interlukin-1 beta were elevated, together with a reduction of interleukin-10 in the liver. In addition, TAA increased hepatic content of transforming growth factor- beta, hydroxyproline, alpha- smooth muscle actin and gene expression of collagen-1. Pretreatment with tadalafil protected against TAA-induced liver fibrosis, in a dose-dependent manner, as proved by the alleviation of inflammatory and fibrotic biomarkers. The effects of tadalafil were comparable with that of silymarin, a natural antioxidant, and could be assigned to its anti-inflammatory and anti-fibrotic properties. Key Words: liver fibrosis, thioacetamide, tadalafil, alpha- smooth muscle actin, collagen-1 expression, interleukin-10, rats.

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