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 Wis...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 β1 （TGF-β1）, 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-β1 （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.展开更多
AIM:To investigate the association of fatty liver and smoking on metabolic syndrome and its components.METHODS:This cross-sectional study enrolled participants who attended annual health screening at Shin Kong Wu Ho-S...AIM:To investigate the association of fatty liver and smoking on metabolic syndrome and its components.METHODS:This cross-sectional study enrolled participants who attended annual health screening at Shin Kong Wu Ho-Su Memorial Hospital from January to December 2005.A total of 3455(1981 men and 1474 women) subjects were included in final analyses.Fatty liver was diagnosed using abdominal ultrasonography by trained gastroenterologists.The modified National Cholesterol Education Program Adult Treatment Panel Ⅲ was used to define metabolic syndrome.The associations between smoking,fatty liver and metabolic syndrome were analyzed using multiple logistic regression.RESULTS:Subjects with fatty liver,and who smoked tobacco,had the highest odds ratios(ORs) for high waist circumference [OR,4.5(95% CI:3.3-6.1) ,P < 0.05],hypertriglyceridemia [OR,8.1(95% CI:6.0-10.9) ,P < 0.05],low serum high-density lipoprotein cholesterol(HDL-C) [OR,8.3(95% CI:6.1-11.3) ,P < 0.05],and metabolic syndrome [OR,9.5(95% CI:6.7-13.4) ,P < 0.05] compared to subjects without fatty liver who did not smoke tobacco.We also found that the ORs for hypertriglyceridemia,low serum HDL-C,and metabolic syndrome for subjects with fatty liver who smoked tobacco had greater than the sum of the ORs for subjects with fatty liver who did not smokeplus those who did not have fatty liver and who did smoke.CONCLUSION:Fatty liver and smoking had a synergistic effect on metabolic syndrome and its components,especially for hypertriglyceridemia and low serum HDL-C.展开更多
文摘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 β1 （TGF-β1）, 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-β1 （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.
文摘AIM:To investigate the association of fatty liver and smoking on metabolic syndrome and its components.METHODS:This cross-sectional study enrolled participants who attended annual health screening at Shin Kong Wu Ho-Su Memorial Hospital from January to December 2005.A total of 3455(1981 men and 1474 women) subjects were included in final analyses.Fatty liver was diagnosed using abdominal ultrasonography by trained gastroenterologists.The modified National Cholesterol Education Program Adult Treatment Panel Ⅲ was used to define metabolic syndrome.The associations between smoking,fatty liver and metabolic syndrome were analyzed using multiple logistic regression.RESULTS:Subjects with fatty liver,and who smoked tobacco,had the highest odds ratios(ORs) for high waist circumference [OR,4.5(95% CI:3.3-6.1) ,P < 0.05],hypertriglyceridemia [OR,8.1(95% CI:6.0-10.9) ,P < 0.05],low serum high-density lipoprotein cholesterol(HDL-C) [OR,8.3(95% CI:6.1-11.3) ,P < 0.05],and metabolic syndrome [OR,9.5(95% CI:6.7-13.4) ,P < 0.05] compared to subjects without fatty liver who did not smoke tobacco.We also found that the ORs for hypertriglyceridemia,low serum HDL-C,and metabolic syndrome for subjects with fatty liver who smoked tobacco had greater than the sum of the ORs for subjects with fatty liver who did not smokeplus those who did not have fatty liver and who did smoke.CONCLUSION:Fatty liver and smoking had a synergistic effect on metabolic syndrome and its components,especially for hypertriglyceridemia and low serum HDL-C.
