Protector efect of HGF in intrahepatic cholestasis

SALAS SILVA E.S.; SIMONI NIEVES A.; BELLO MONROY O.; BUCIO ORTÍZ L.; ROMA M.G.; GÓMEZ QUIROZ L.E.; GUTIÉRREZ RUÍZ M.C.

Mérida

Congreso; XII Congreso Nacional de Hepatología de la Asociación Mexicana de Hepatología; 2017

Asociación Mexicana de Hepatología

Introduction.Cholestasis is a common syndrome in a large number of hepatic diseases,such as drug-induced cholestasis which is produced due to a primary lesion ofthe bile conducts either functional or obstructive, generating oxidative stressin the liver. Hepatocyte growth (HFG) factor, and its receptor, c-Met,represents the first defense line against hepatotoxics factors because they inducethe Nrf2 activation which, in turn, will activate its target genes to lead toan antioxidant and repair response. The aim of this research is to characterizethe anticholestatic molecular and cellular mechanism measured with the HGF in a(urine model of inflammatory cholestasis induced by the α-naftil-isotiocianato(ANIT).Materialand methods. CD1 Mice were used, treated with anaftil isotiocianato(60 μg/kg)for 48 h intragastricaly. After 24 h of ANIT, HGF (10 μg/kg) wereadministrated intravenously. When 48 h passed the sacrifice were done wherebybiochemist tests were undertaken such as AST, ALT, ALP and H-E staining.Similarly mouse hepatocytes were obtained for primary culture which were treatedwith ANIT (20 μM)and HGF (50 ng) in order to carry out viability and functionality tests.Results.Animales treated with ANIT present liver injury, (hepatomegalia) andcholecystitis, those effects were reverted when HGF was administrated incomparison with the ones that were just damaged. In the ANIT treated cellularculture we could observe a decrease in the cellular viability as well as in itsfunctionality, however when the culture was pre-treated with HGF it wasobserved that the cellular viability was kept even though it was exposed toANIT.Conclusion.Data shows that HGF treated animals improved significantly in comparisonwith the ANIT damaged, besides HGF provides cellular dead protection inhepatocytes primary culture. Based on this we can considere HGF as atherapeutic intervention point in cholestatic diseases.