Protective effects of total saponins of Panax japonicas on non-alcoholic fatty liver disease through regulating expression of miR-199-5p.
10.19540/j.cnki.cjcmm.20180606.001
- Author:
Hai-Rong XIONG
1
;
Cong LI
1
;
Chun-Xi HE
2
;
Yu-Min HE
2
;
Cheng-Fu YUAN
2
;
Ting WANG
2
;
Chang-Cheng ZHANG
2
;
Ding YUAN
2
;
Chao-Qi LIU
1
Author Information
1. Hubei Key Laboratory of Tumor Microenvironment and Immunotheraphy, Three Gorges University， Yichang 443002, China.
2. Medical College， Three Gorges University， Yichang 443002， China.
- Publication Type:Journal Article
- Keywords:
HGF;
c-Met;
miR-199-5p;
nonalcoholic fatty liver disease;
total saponins of Panax japonicas
- From:
China Journal of Chinese Materia Medica
2018;43(17):3525-3529
- CountryChina
- Language:Chinese
-
Abstract:
To research the effection and probable mechanism for the total saponins of Panax japonicas(TPSJ) in mice on non-alcoholic fatty liver disease. Forty SPF male Kunming mice were randomily divided into four group:control group,NAFLD group, low-dose TPSJ treated group,high-dose TPSJ treated group. High-fatty and high-frutose-diet was applied to eatablish NAFLD model，and TPSJ (100 and 200 mg·kg⁻¹) in feeding were given for the TPSJ groups for 4 weeks. To collect the serum with liver and the ALT and TC of serum were monitored after 4 weeks. The hepatic histopathologic structure was observed by haematoxylin-eosin (HE) staining, RT-PCR and RT-qPCR was applied for the detection of miR-199-5p，VEGFa，HGF，c-Met and protein expression level was detected bv laser confocal microscope.Compared with control group, the level of serum ALT and TC in the model group was higher,the liver of the model group showed that hepatocytes display obvious lipid deposition. Then TPSJ treated showed that markedly improved histopathologic changes, decreased fatty deposition. In the meantime,the expression level of miR-199-5p was significantly decreased, thus the expression of HGF and c-Met were significantly increased. TPSJ play a role of prevention on fatty liver, the machanism maybe by blocking miR-199-5p targeted to c-Met signaling pathways in NAFLD.
