an investigation of the hepatoprotective effect of coleus vettiveroides ethanolic root extract against thioacetamide induced acute and chronic liver injury in rats

Abstract

Liver diseases are responsible for more than 10 million annual deaths worldwide. newlineMany people are currently affected with any one of the chronic liver injuries such newlineas non-alcoholic fatty liver diseases, alcoholic fatty liver diseases, fibrosis, newlinecirrhosis, and hepatocellular carcinoma (HCC). The currently available, newlinepharmacological treatment options for liver diseases are limited, expensive, and newlineineffective. Hence, the overall aim of this study was to evaluate the newlinehepatoprotective properties effect of Coleus vettiveroides ethanolic root extract newline(CVERE) against thioacetamide (TAA)-induced acute and chronic liver injury in newlineWistar albino rats. newline2.2 OBJECTIVES newlineThe objectives of present study are newlineand#61656; To investigate the qualitative and quantitative evaluation of newlinephytochemicals present in the CVERE newlineand#61656; To investigate the acute oral toxicity analysis of CVERE in Wistar rats newlineand#61656; To investigate the sub-acute oral toxicity analysis of CVERE in Wistar rats newlineand#61656; To investigate the apoptosis inducing and cell cycle arresting potentials of newlineCVERE in vitro using HepG2 cells, an HCC cell line. newlineand#61656; To investigate the influence of CVERE on TAA-induced acute liver injury newlinein rats newlineand#61656; To investigate the influence of CVERE on TAA-induced chronic liver injury newlinein rats newline12 newline2.3 HYPOTHESIS newlineThe epidemiological studies have estimated gt1 million HCC cases by 2025. HCC newlineis the most common form of liver cancer and accounts for ~90% of cases. HCC newlineis said to commence due to uncontrolled proliferation and apoptosis-resistance in newlinecancer cells. It is likely that CVERE treatment could either retard proliferation by newlinearresting cell cycle or by inducing apoptosis in HepG2 cells. Hence, the probable newlinemechanism of CVERE-mediated inhibition of HepG2 proliferation, if any, was newlineinvestigated in vitro by using HepG2 cells. newlineTAA administration causes oxidative stress and inflammation in the liver via newlinereactive metabolites production during their biotransformation in the liver. It is newlinehypothesized that TAA hepatotoxicity occurs due to oxidant-antioxidan