Hong-Shan Li1, Qin Feng, Li-Li Xu, Shao-Dong Chen, Xue-Mei Li, Yi-Yang Hu. 1. Institute of Liver Diseases of Shuguang Hospital, Key Laboratory for Liver-Kidney Disease Pattern of Ministry of Education, E-Institute of Shanghai Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.
Abstract
OBJECTIVE: To explore the effects of Qushi Huayu Decoction (QSHYD), a compound traditional Chinese herbal medicine, in prevention and treatment of non-alcoholic fatty liver disease (NAFLD) in rats. METHODS: Forty Wistar male rats were used to establish the NAFLD model by subcutaneous injection of carbon tetrachloride (CCl(4)) for 4 weeks (twice weekly) along with high-fat and low-protein diet for 2 weeks. After two-week administration, the rats were randomly divided into four groups: untreated group, high-dose QSHYD group, medium-dose QSHYD group and low-dose QSHYD group. Another six rats were used as normal control. After 2-week treatment, the following indexes were detected: (1) liver pathology; (2) contents of serum adiponectin (ADP) and liver triglyceride (TG); (3) concentrations of liver FFA, adiponectin receptor 2 (AdipoR2), malonyl-coenzyme A (malony1-CoA), AMP-activated protein kinase (AMPK), acetyl-CoA carboxylase (ACCase), fatty acid synthase (FAS) and carnitine palmitoyl transferase-1 (CPT-1). RESULTS: Compared with the normal group, there were physiological changes associated with hepatic steatosis and inflammation in liver tissues in the untreated group as observed by oil red O staining and HE staining. The TG, FFA, malony1-CoA, FAS, and ACCase concentrations in liver tissues in the untreated group were elevated significantly. While the contents of ADP in serum and AdipoR2, CPT-1 and AMPK in liver tissues in the untreated group were decreased markedly. The pathological damages in each QSHYD-treated group were significantly less than those in the untreated group. The TG and FFA contents in liver tissues in each QSHYD-treated group were significantly decreased. The FAS, ACCase and malonyl-CoA concentrations in liver tissues of the high QSHYD-treated group were reduced markedly as compared with the untreated group. High- and medium-dose of QSHYD could significantly increase ADP content in serum and AMPK, CPT-1 and AdipoR2 contents in liver tissues. CONCLUSION: QSHYD can affect the ADP-FFA pathway by increasing the content of serum ADP, which may be one of its important mechanisms in preventing and treating NAFLD in rats.
OBJECTIVE: To explore the effects of Qushi Huayu Decoction (QSHYD), a compound traditional Chinese herbal medicine, in prevention and treatment of non-alcoholic fatty liver disease (NAFLD) in rats. METHODS: Forty Wistar male rats were used to establish the NAFLD model by subcutaneous injection of carbon tetrachloride (CCl(4)) for 4 weeks (twice weekly) along with high-fat and low-protein diet for 2 weeks. After two-week administration, the rats were randomly divided into four groups: untreated group, high-dose QSHYD group, medium-dose QSHYD group and low-dose QSHYD group. Another six rats were used as normal control. After 2-week treatment, the following indexes were detected: (1) liver pathology; (2) contents of serum adiponectin (ADP) and liver triglyceride (TG); (3) concentrations of liver FFA, adiponectin receptor 2 (AdipoR2), malonyl-coenzyme A (malony1-CoA), AMP-activated protein kinase (AMPK), acetyl-CoA carboxylase (ACCase), fatty acid synthase (FAS) and carnitine palmitoyl transferase-1 (CPT-1). RESULTS: Compared with the normal group, there were physiological changes associated with hepatic steatosis and inflammation in liver tissues in the untreated group as observed by oil red O staining and HE staining. The TG, FFA, malony1-CoA, FAS, and ACCase concentrations in liver tissues in the untreated group were elevated significantly. While the contents of ADP in serum and AdipoR2, CPT-1 and AMPK in liver tissues in the untreated group were decreased markedly. The pathological damages in each QSHYD-treated group were significantly less than those in the untreated group. The TG and FFA contents in liver tissues in each QSHYD-treated group were significantly decreased. The FAS, ACCase and malonyl-CoA concentrations in liver tissues of the high QSHYD-treated group were reduced markedly as compared with the untreated group. High- and medium-dose of QSHYD could significantly increase ADP content in serum and AMPK, CPT-1 and AdipoR2 contents in liver tissues. CONCLUSION: QSHYD can affect the ADP-FFA pathway by increasing the content of serum ADP, which may be one of its important mechanisms in preventing and treating NAFLD in rats.