Abstract
Lentinus edodes is the medicinal macrofungus showing potential for therapeutic applications in infectious disorders including hepatitis. In an attempt to develop the agent for handling hepatic injury, we used the extracts of Lentinus edodes mycelia (LEM) to screen the effect on hepatic injury in rats induced by carbon tetrachloride (CCl4). Intraperitoneal administration of CCl4 not only increased plasma glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) but also decreased hepatic superoxide dismutase (SOD) and glutathione peroxidase (GPx) levels in rats. Similar to the positive control silymarin, oral administration (three times daily) of this product (LEM) for 8 weeks significantly reduced plasma GOT and GPT. Also, the activities of antioxidant enzymes of SOD and GPx were elevated by LEM. in liver from CCl4-treated rats, indicating that mycelium can increase antioxidant-like activity. Moreover, the hepatic mRNA and protein levels of SOD and GPx were both markedly raised by LEM. The obtained results suggest that oral administration of the extracts of Lentinus edodes mycelia (LEM) has the protective effect against CCl4-induced hepatic injury in rats, mainly due to an increase in antioxidant-like action.
Highlights
Hepatic injury may result from many risk factors, such as hepatic virus, inflammation, and alcohol consumption [1,2,3]
We screen the extracts of Lentinus edodes mycelia (LEM) in rats using Carbon tetrachloride- (CCl4-)induced liver damage model while silymarin is used as a positive control because it is popularly applied as the protective substance in CCl4-induced hepatic damage [14, 15]
We found that the extracts of Lentinus edodes mycelia (LEM) can significantly lower plasma glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) in CCl4-treated rats
Summary
Hepatic injury may result from many risk factors, such as hepatic virus, inflammation, and alcohol consumption [1,2,3]. Carbon tetrachloride- (CCl4-) induced hepatic injury is a well-established animal model due to generation of oxidative stress to result in hepatic oxidative damage and inflammation [6]. CCl4-induced hepatic injury is a common animal model widely used to evaluate the hepatoprotective action of testing compounds [7,8,9]. Protection of LEM against liver damage induced by chemicals has been documented such as dimethylnitrosamine [12] and Dgalactosamine [13]. Both reports were carried out in cultured hepatic cells. The main aim of the present study is going to clarify the role of antioxidant-like activity in the liver protection of this product (LEM)
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