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. 2012:2012:231586.
doi: 10.1100/2012/231586. Epub 2012 May 22.

Protection of the extracts of Lentinus edodes mycelia against carbon-tetrachloride-induced hepatic injury in rats

Mei-Fen Chen  1 , Hsien-Hui Chung, Han-Lin Lu
Affiliations

Protection of the extracts of Lentinus edodes mycelia against carbon-tetrachloride-induced hepatic injury in rats

Mei-Fen Chen et al. ScientificWorldJournal. 2012.

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.

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Figures

Figure 1
Figure 1
Effect of LEM on hepatic injury in CCl4-treated rats. All rats were received oral administration at indicated dose three times per day. (a) Normal rats treated with vehicle. (b) Normal rats treated with CCl4 for 8 weeks. (c) CCl4-treated rats received oral administration of silymarin (200 mg/kg) for 8 weeks. (d) CCl4-treated rats received oral administration of LEM (100 mg/kg) for 8 weeks. (e) CCl4-treated rats received oral administration of LEM (200 mg/kg) for 8 weeks. (f) CCl4-treated rats received oral administration of LEM (500 mg/kg) for 8 weeks. Histology of liver was characterized by staining with hematoxylin-eosin (Magnification: ×400).
Figure 2
Figure 2
Effect of LEM on plasma GOT and GPT levels in CCl4-treated rats. (a) Changes of plasma GOT by oral administration of LEM in CCl4-treated rats for 8 weeks. (b) Changes of plasma GPT by oral administration of LEM in CCl4-treated rats for 8 weeks. Lane 1: vehicle-treated Wistar rats; lane 2: vehicle-treated CCl4-induced rats; lane 3: silymarin- (200 mg/kg) treated CCl4-induced rats; lane 4: LEM- (100 mg/kg) treated CCl4-induced rats; lane 5: LEM- (200 mg/kg) treated CCl4-induced rats; lane 6: LEM- (500 mg/kg) treated CCl4-induced rats. Data represent mean ± SEM of eight animals. *P < 0.05, **P < 0.01, and ***P < 0.001 compared with CCl4-induced group receiving vehicle.
Figure 3
Figure 3
Effects of LEM on activities of hepatic Mn-SOD, Cu/Zn-SOD, and glutathione peroxidase (GPx) in CCl4-treated rats. (a) Changes of hepatic Mn-SOD by oral administration of LEM in CCl4-treated rats for 8 weeks. (b) Changes of hepatic Cu/Zn-SOD by oral administration of LEM in CCl4-treated rats for 8 weeks. (c) Changes of hepatic GPx by oral administration of LEM in CCl4-treated rats for 8 weeks. Lane 1: vehicle-treated Wistar rats; lane 2: vehicle-treated CCl4-induced rats; lane 3: silymarin- (200 mg/kg) treated CCl4-induced rats; lane 4: LEM- (100 mg/kg) treated CCl4-induced rats; lane 5: LEM- (200 mg/kg) treated CCl4-induced rats; lane 6: LEM- (500 mg/kg) treated CCl4-induced rats. Data represent mean ± SEM of eight animals. * P < 0.05 and ** P < 0.01 compared with CCl4-induced group receiving vehicle.
Figure 4
Figure 4
Effects of LEM on gene expressions of Mn-SOD, Cu/Zn-SOD, and glutathione peroxidase (GPx) in liver of CCl4-treated rats. (a) The representative picture showing mRNA levels for Mn-SOD, Cu/Zn-SOD, GPx, or β-actin in liver isolated from CCl4-induced rats receiving treatment with silymarin or LEM three times daily for 8 weeks. Lane 1: vehicle-treated Wistar rats; lane 2: vehicle-treated CCl4-induced rats; lane 3: silymarin- (200 mg/kg) treated CCl4-induced rats; lane 4: LEM- (100 mg/kg) treated CCl4-induced rats; lane 5: LEM- (200 mg/kg) treated CCl4-induced rats; lane 6: LEM- (500 mg/kg) treated CCl4-induced rats. (b) The representative response of protein level for Mn-SOD, Cu/Zn-SOD, GPx, or actin in liver isolated from CCl4-induced rats receiving treatment with silymarin or LEM three times daily for 8 weeks. All lanes are expressed as the same as mRNA level (a) on the above.
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