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Ameliorative effect of Ganoderma lucidum on carbon tetrachloride-induced liver fibrosis in rats
1Department of Pharmacology, China Medical University, 91 Hsueh Shih Road, Taichung 404, Taiwan, China. wclin@mail.cmu.edu.tw
Aim:
To investigate the effects of Reishi mushroom, Ganoderma lucidum extract (GLE), on liver fibrosis induced by carbon tetrachloride (CCl4) in rats.
Methods:
Rat hepatic fibrosis was induced by CCl4. Forty Wistar rats were divided randomly into 4 groups: control, CCl4, and two GLE groups. Except for rats in control group, all rats were administered orally with CCl4 (20%, 0.2 mL/100 g body weight) twice a week for 8 weeks. Rats in GLE groups were treated daily with GLE (1,600 or 600 mg/kg) via gastrogavage throughout the whole experimental period. Liver function parameters, such as ALT, AST, albumin, and albumin/globulin (A/G) ratio, spleen weight and hepatic amounts of protein, malondiladehyde (MDA) and hydroxyproline (HP) were determined. Histochemical staining of Sirius red was performed. Expression of transforming growth factor beta1 (TGF-beta1), methionine adenosyltransferase (MAT1) 1A and MAT2A mRNA were detected by using RT-PCR.
Results:
CCl4 caused liver fibrosis, featuring increase in plasma transaminases, hepatic MDA and HP contents, and spleen weight; and decrease in plasma albumin, A/G ratio and hepatic protein level. Compared with CCl4 group, GLE (600, 1,600 mg/kg) treatment significantly increased plasma albumin level and A/G ratio (P < 0.05) and reduced the hepatic HP content (P < 0.01). GLE (1,600 mg/kg) treatment markedly decreased the activities of transaminases (P < 0.05), spleen weight (P < 0.05) and hepatic MDA content (P < 0.05); but increased hepatic protein level (P < 0.05). Liver histology in the GLE (1,600 mg/kg)-treated rats was also improved (P < 0.01). RT-PCR analysis showed that GLE treatment decreased the expression of TGF-beta1 (P < 0.05-0.001) and changed the expression of MAT1A (P < 0.05-0.01) and MAT2A (P < 0.05-0.001).
Conclusion:
Oral administration of GLE significantly reduces CCl4-induced hepatic fibrosis in rats, probably by exerting a protective effect against hepatocellular necrosis by its free-radical scavenging ability.
