Objective： To observe the effect of berberine on uncoupling protein-2 （UCP2） mRNA and protein expressions in the hepatic tissue of non-alcoholic fatty liver disease （NAFLD） in rats, and to explore the molecular m...Objective： To observe the effect of berberine on uncoupling protein-2 （UCP2） mRNA and protein expressions in the hepatic tissue of non-alcoholic fatty liver disease （NAFLD） in rats, and to explore the molecular mechanism. Methods： To establish the NAFLD rat model; the rats were fed by high fat forage and were randomly divided into four groups： normal group, model group, berberine high-dose group （324 mg/ kg）, and berberine low-dose group （162 mg/kg）. After treatment for 12 weeks, the expression of UCP2 mRNA in the liver tissue was analyzed by semiquantitative reverse transcription polymerase chain reaction （RTPCR）. The expression level of UCP2 protein in the liver tissue was examined by immunohistochemistry. Total cholesterol （TC）, triglyceride （TG）, high-density lipoprotein cholesterol （HDL-C）, and low-density lipoprotein cholesterol （LDL-C） contents in blood serum, and TG and TC contents in the liver were detected by an automatic biochemical analyzer. The other is to observe the axungia degree of the liver. Results： The expression of UCP2 mRNA and positive cell numbers in the liver tissue were dramatically increased in the model group （P〈0.01）. Lipid in the serum and hepatic tissues increased significantly, and the liver was fatty. But in the treatment groups, the expression levels of mRNA and UCP2 proteins were significantly down-regulated （P〈0.01）. Liver steatosis was improved. Conclusions： Berberine can down-regulate the expression levels of UCP2 mRNA and UCP2 proteins of hepatic tissue in NAFLD rats. It can promote the recovery of hepatocyte steatosis and improve lipid metabolism disorder in NAFLD rats. Berberine shows a potential therapeutic effect on NAFLD.展开更多
Objective： To observe the effects of different therapeutic methods and the recipes of Chinese medicine （CM） on the activation of c-Jun N-terminal kinase （JNK） in Kupffer cells of rats with fatty liver disease and...Objective： To observe the effects of different therapeutic methods and the recipes of Chinese medicine （CM） on the activation of c-Jun N-terminal kinase （JNK） in Kupffer cells of rats with fatty liver disease and to explore the mechanisms of these therapeutic methods. Methods： By using a random number table, 98 rats were randomly divided into 7 groups： control group, model group, and 5 treatment groups, including soothing Liver （Gan） recipe group, invigorating Spleen （Pi） recipe group, dispelling dampness recipe group, promoting blood recipe group, and complex recipe group. Rats in the control group were fed with normal food and distilled water by gastric perfusion, while rats in the model group were fed with high-fat food and distilled spirits by gastric perfusion. Rats in the 5 treatment groups were fed with high-fat food and corresponding recipes by gastric perfusion. Twelve weeks later, all rats were sacrificed and liver tissues were stained for pathohistological observation. Kupffer cells were isolated from livers of rats to evaluate JNK and phospho-JNK expressions by Western blotting. Results： The grade of hepatic steatosis was higher in the model group than the control group （P〈0.05）. Compared with the model group, the grade of fatty degeneration in soothing Liver recipe group and invigorating Spleen recipe group were significantly ameliorated （P〈0.05）. Expressions of JNK and phospho-JNK in Kupffer cells were significantly higher in the model group than those in the control group （P〈0.05, P〈0.01）. Compared with the model group, expressions of JNK in all treatment groups decreased, especially in invigorating Spleen recipe group and promoting blood recipe group （P〈0.05）. Compared with the model group, expressions of phospho-JNK in all treatment groups declined significantly （P〈0.01）, especially in soothing Live recipe group and invigorating Spleen recipe group. Conclusions： The high expressions of JNK and phospho-JNK in Kupffer cells might play an imp展开更多
文摘Objective： To observe the effect of berberine on uncoupling protein-2 （UCP2） mRNA and protein expressions in the hepatic tissue of non-alcoholic fatty liver disease （NAFLD） in rats, and to explore the molecular mechanism. Methods： To establish the NAFLD rat model; the rats were fed by high fat forage and were randomly divided into four groups： normal group, model group, berberine high-dose group （324 mg/ kg）, and berberine low-dose group （162 mg/kg）. After treatment for 12 weeks, the expression of UCP2 mRNA in the liver tissue was analyzed by semiquantitative reverse transcription polymerase chain reaction （RTPCR）. The expression level of UCP2 protein in the liver tissue was examined by immunohistochemistry. Total cholesterol （TC）, triglyceride （TG）, high-density lipoprotein cholesterol （HDL-C）, and low-density lipoprotein cholesterol （LDL-C） contents in blood serum, and TG and TC contents in the liver were detected by an automatic biochemical analyzer. The other is to observe the axungia degree of the liver. Results： The expression of UCP2 mRNA and positive cell numbers in the liver tissue were dramatically increased in the model group （P〈0.01）. Lipid in the serum and hepatic tissues increased significantly, and the liver was fatty. But in the treatment groups, the expression levels of mRNA and UCP2 proteins were significantly down-regulated （P〈0.01）. Liver steatosis was improved. Conclusions： Berberine can down-regulate the expression levels of UCP2 mRNA and UCP2 proteins of hepatic tissue in NAFLD rats. It can promote the recovery of hepatocyte steatosis and improve lipid metabolism disorder in NAFLD rats. Berberine shows a potential therapeutic effect on NAFLD.
基金Supported by the National Natural Science Foundation of China (No.30371726)
文摘Objective： To observe the effects of different therapeutic methods and the recipes of Chinese medicine （CM） on the activation of c-Jun N-terminal kinase （JNK） in Kupffer cells of rats with fatty liver disease and to explore the mechanisms of these therapeutic methods. Methods： By using a random number table, 98 rats were randomly divided into 7 groups： control group, model group, and 5 treatment groups, including soothing Liver （Gan） recipe group, invigorating Spleen （Pi） recipe group, dispelling dampness recipe group, promoting blood recipe group, and complex recipe group. Rats in the control group were fed with normal food and distilled water by gastric perfusion, while rats in the model group were fed with high-fat food and distilled spirits by gastric perfusion. Rats in the 5 treatment groups were fed with high-fat food and corresponding recipes by gastric perfusion. Twelve weeks later, all rats were sacrificed and liver tissues were stained for pathohistological observation. Kupffer cells were isolated from livers of rats to evaluate JNK and phospho-JNK expressions by Western blotting. Results： The grade of hepatic steatosis was higher in the model group than the control group （P〈0.05）. Compared with the model group, the grade of fatty degeneration in soothing Liver recipe group and invigorating Spleen recipe group were significantly ameliorated （P〈0.05）. Expressions of JNK and phospho-JNK in Kupffer cells were significantly higher in the model group than those in the control group （P〈0.05, P〈0.01）. Compared with the model group, expressions of JNK in all treatment groups decreased, especially in invigorating Spleen recipe group and promoting blood recipe group （P〈0.05）. Compared with the model group, expressions of phospho-JNK in all treatment groups declined significantly （P〈0.01）, especially in soothing Live recipe group and invigorating Spleen recipe group. Conclusions： The high expressions of JNK and phospho-JNK in Kupffer cells might play an imp
