Abstract
Licorice has been used in Chinese folk medicine for the treatment of various disorders. Licorice has the biological capabilities of detoxication, antioxidation, and antiinfection. In this study, we evaluated the antihepatotoxic effect of licorice aqueous extract (LE) on the carbon tetrachloride (CCl4)-induced liver injury in a rat model. Hepatic damage, as reveled by histology and the increased activities of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) activities, and decreased levels of serum total protein (TP), albumin (Alb) and globulin (G) were induced in rats by an administration of CCl4 at 3 mL/kg b.w. (1:1 in groundnut oil). Licorice extract significantly inhibited the elevated AST, ALP and ALT activities and the decreased TP, Alb and G levels caused by CCl4 intoxication. It also enhanced liver super oxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR), Glutathione S-transferase (GST) activities and glutathione (GSH) level, reduced malondialdehyde (MDA) level. Licorice extract still markedly reverses the increased liver hydroxyproline and serum TNF-α levels induced by CCl4 intoxication. The data of this study support a chemopreventive potential of licorice extract against liver oxidative injury.
Highlights
Liver is the key organ of metabolism and excretion
Treatment with CCl4 generates free radicals that trigger a cascade of events that result in hepatic fibrosis, mimicking the oxidative stress that has a fibrogenic effect on HSC [2,3,4]
Toxicity test showed that 15 days of licorice aqueous extract (LE) treatment did not significantly affect rats’ final body weight
Summary
It is often exposed to a variety xenobiotics and therapeutic agents. People have not yet found an actual curative therapeutic agent for liver disorder. Most of the available remedies help the healing or regeneration of the liver. The hepatotoxin carbon tetrachloride (CCl4) is frequently used to induce liver fibrosis in animal models [1]. Treatment with CCl4 generates free radicals that trigger a cascade of events that result in hepatic fibrosis, mimicking the oxidative stress that has a fibrogenic effect on HSC [2,3,4]. No successful therapeutic approach to this pathogenetic mechanism in liver disease has been developed, antioxidants therapies have shown to achieve some positive effects [6,7,8]
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