Effects of Extracted Active Components of Chaenomeles Speciosa on Non-alcoholic Fatty Liver Disease in Model Mice induced by High-fat–high-fructose Diet
10.3969/j.issn.1005-5304.2017.05.012
- VernacularTitle:木瓜提取物对高糖高脂诱导的小鼠非酒精性脂肪性肝病的影响
- Author:
Lichun WU
;
Hao TU
;
Li DUAN
;
Huiyu SHE
;
Wei ZHANG
;
Changcheng ZHANG
;
Ding YUAN
;
Chaoqi LIU
- Keywords:
Chaenomeles Speciosa extracts;
non-alcoholic fatty liver disease;
lipid metabolism;
SIRT1 signaling pathway;
mice
- From:
Chinese Journal of Information on Traditional Chinese Medicine
2017;24(5):48-51
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the effects of extracted active components of Chaenomeles Speciosa (EACCS) on non-alcoholic fatty liver disease (NAFLD) in mice; To discuss the possible molecular mechanism. Methods Forty male KM mice were randomized into four groups, namely normal group, model group, low-dose (50 mg/kg) EACCS group and high-dose (100 mg/kg) EACCS group. Except that the normal group was daily given routine diet, the other groups were given high-fat–high-fructose diet (HFFD). The mice were put to death 4 weeks later. Body weight, liver weight and serum TG were measured. HE and oil red O staining were used to observe liver tissue morphology. RT-PCR and Western blot were used to detect the expression of lipid metabolism related genes. Results Compared with the normal group, the liver size, liver index (P<0.01) and epididymal fat index (P<0.05) increased significantly;The ALT and GLU in serum increased (P<0.05), TG increased (P<0.05), and pathological findings showed significant steatosis; RT-PCR and Western blot showed that the expression levels of SIRT1 and FoxO1 mRNA decreased and the level of SERBP-1c increased in the model group. Compared with the model group, the hepatic lipid accumulation of EACCS groups was obviously improved, and the serum ALT, GLU, and TG levels significantly decreased, the expression levels of hepatic SIRT1 and FoxO1 mRNA increased. Conclusion EACCS has protective effects on NAFLD mice induced by HFFD, and its mechanism may be related to the activation of SIRT1-FoxO1 signaling pathway in the liver tissues.
