Abstract
Elephantopus scaber has been traditionally used as liver tonic. However, the protective effect of E. scaber on ethanol-induced liver damage is still unclear. In this study, we have compared the in vivo hepatoprotective effect of E. scaber with Phyllanthus niruri on the ethanol-induced liver damage in mice. The total phenolic and total flavanoid content of E. scaber ethanol extract were determined in this study. Accelerating serum biochemical profiles (including AST, ALT, ALP, triglyceride, and total bilirubin) associated with fat drop and necrotic body in the liver section were observed in the mice treated with ethanol. Low concentration of E. scaber was able to reduce serum biochemical profiles and the fat accumulation in the liver. Furthermore, high concentration of E. scaber and positive control P. niruri were able to revert the liver damage, which is comparable to the normal control. Added to this, E. scaber did not possess any oral acute toxicity on mice. These results suggest the potential effect of this extract as a hepatoprotective agent towards-ethanol induced liver damage without any oral acute toxicity effect. These activities might be contributed, or at least in part, by its high total phenolic and flavonoid contents.
Highlights
Reactive oxygen species (ROS) are continuously generated during metabolic processes to regulate a number of physiological functions essential to the body [1]
Our results indicated that the total phenolic content of E. scaber was 193.05 ± 1.17 mg GAE/g of the extract. while the total flavonoid content was 120.87 ± 0.61 mg CE/g of extract
Ethanol treatment resulted in a significant elevation of serum alanine transaminase (ALT), alkaline phosphatase (ALP), and aspartate transaminase (AST) levels in comparison to the control group (Table 2)
Summary
Reactive oxygen species (ROS) are continuously generated during metabolic processes to regulate a number of physiological functions essential to the body [1]. When the production of ROS exceeds the capability of the body to detoxify these reactive intermediates, oxidative stress would be generated [2]. This may lead to drastic harm to the body such as membrane damage, mutations due to attenuation of DNA molecules, and disruption to various enzymatic activities in metabolism of the body [3,4,5]. Metabolism of alcohol in liver generates excessive free radicals and increased peroxisomal oxidation of fatty acid, which would affect functionality of the antioxidant systems to eliminate ROS in the body [6]. The mechanism to restore hepatic injuries caused by alcoholic oxidative stress is tightly regulated by the antioxidant status of a living system
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