Protein Information

ID 1425
Name adiponectin
Synonyms 30 kDa adipocyte complemen related protein; 30 kDa adipocyte complement related protein; ACDC; ACRP30; ADIPOQ; APM 1; APM1; Adipocyte C1Q and collagen domain containing…

Compound Information

ID 1392
Name carbon tetrachloride
CAS tetrachloromethane

Reference

PubMed Abstract RScore(About this table)
19583937 Li HS, Feng Q, Xu LL, Chen SD, Li XM, Hu YY: [Effects of Qushi Huayu Decoction in prevention and treatment of fatty liver in rats based on adiponection-free fatty acid pathway]. Zhong Xi Yi Jie He Xue Bao. 2009 Jun;7(6):546-51.
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.
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