Evaluation of Ginger Oleoresin in Carbon Tetrachloride Induced Hepatotoxicity in Rats

Ravinder Khatri Ravinder Khatri,Arvind Sharma Arvind Sharma,Umesh Chettri Umesh Chettri,Srijana Tamang Srijana Tamang,Kiran Kiran,Akshay Sharma Akshay Sharma,Kashish Bhardwaj Kashish Bhardwaj

doi:10.15415/jptrm.2018.62007

Ravinder Khatri Ravinder Khatri, Arvind Sharma Arvind Sharma + Show 5 more

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https://doi.org/10.15415/jptrm.2018.62007

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Abstract

The present study evaluated the hepatoprotective activity of ginger oleoresin against Carbontetrachloride induced liver toxic damage in rats. Rats were divided into six groups. Hepatotoxicity was induced by the administration of a single intraperitoneal dose (2ml/kg) of Carbontetrachloride in experimental rats. Post-treatment with Ginger oleoresin at 300 and 600mg/kg dose given by oral routewas carried out to find their protective effectsagainst carbontetrachloride induced hepatic injury. Biochemical parameterfor oxidative stress, inflammation and lipid profile along with genotoxicity and histological changes in rat serum and liver were studied. Silymarin was used as standard hepatoprotective agent. Extracted oleoresin dose dependently provided hepatoprotective effects.The hepatoprotective action of ginger oleoresin may be related to its free radical scavenging,anti-inflammatory and hypolipidemic activity and concluded to be partly mediated by its active constituent’s 6-gingerol, shogaol and zingerone. -phospate; CCl3 *, Trichloromethyl free radical; CCl3 OO*, Trichloromethyl peroxy radical; ROS, Reactive oxygen species; iNOS, inducible nitric oxide synthase; NO, Nitric oxide, VLDL, Very low density lipoprotein.

Highlights

Liver is the largest gland of body that plays a pivotal role in regulating various physiological processes in the body such as metabolism, secretion and storage
The present study evaluated the hepatoprotective activity of ginger oleoresin against Carbontetrachloride induced liver toxic damage in rats
CCl4 causes the activation of immune system through the infiltration of inflammatory cells to the site of injury, responsible for the release of pro-inflammatory cytokines such as tumor necrosis factor- α (TNF-α), interleukin-6 (IL-6) and c-reactive protein (CRP), which further enhance hepatotoxicity through repeated cycle of inflammation (Mohamed et al, 2001a)

Summary

Introduction

Liver is the largest gland of body that plays a pivotal role in regulating various physiological processes in the body such as metabolism, secretion and storage. Lipid peroxidation induce membrane disintegration of liver hepatocytes, which in turn increases the release of cytosolic enzymes such as aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) (Suzek et al, 2015; Mohamed et al, 2014). CCl4 causes the activation of immune system through the infiltration of inflammatory cells to the site of injury, responsible for the release of pro-inflammatory cytokines such as tumor necrosis factor- α (TNF-α), interleukin-6 (IL-6) and c-reactive protein (CRP), which further enhance hepatotoxicity through repeated cycle of inflammation (Mohamed et al, 2001a). CCl4 induced hepatotoxicity lead toaccumulation of Ca2+ in mitochondria, activate many membrane damaging enzymes, causes disruption of mitochondrial metabolism, decreased ATP synthesis and damage micro-filaments that support cell structure(Deepa et al, 2013; Nicotera et al, 1990).

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