Effect and Mechanism of Xiangsha Liujunzi Tang on Lipid Deposition in Liver of ApoE-/- AS Mice by Affecting Long Noncoding RNA-HC/miR-130b and to Regulate Cholesterol Metabolism
10.13422/j.cnki.syfjx.20202304
- VernacularTitle:香砂六君子汤调控长链非编码RNA-HC/miR-130b调节胆固醇代谢对ApoE-/- AS小鼠肝脏脂质沉积的影响及机制
- Author:
Si CHEN
1
;
Nan SONG
1
;
Ying WANG
1
;
Hui-min CAO
1
;
Xiao YANG
2
;
Fang YANG
2
;
Qun WANG
1
;
Lian-qun JIA
1
Author Information
1. Chinese Medicine Innovation Engineering Technology Center， Liaoning Key Laboratory of Ministry of Education for Traditional Chinese Medicine （TCM） Viscera-State Theory and Applications，Liaoning University of TCM， Shenyang 110847， China
2. The Second Affiliated Hospital of Liaoning University of TCM， Shenyang 110034， China
- Publication Type:Research Article
- Keywords:
long noncoding RNA-HC;
ApoE-/- atherosclerotic （AS） mice;
cholesterol metabolism;
Xiangsha Liujunzi Tang
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2021;27(3):15-21
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the mechanism of Xiangsha Liujunzi Tang in improving liver lipid deposition in ApoE-/- atherosclerotic （AS） mice by affecting long noncoding RNA-HC （Lnc-HC）/microRNA-130b （miR-130b） in the regulation of cholesterol metabolism. Method:Totolly 10 C57BL/6J mice were selected as normal controls， and 30 healthy ApoE-/- mice fed with high fat diet for 12 weeks were then randomly divided into the model group， Xiangsha Liujunzi Tang group（19.12 g·kg-1·d-1） and simvastatin group（2.275 mg·kg-1·d-1）， with gavage administration for 4 weeks. The serum lipid level of mice was detected by automatic biochemistry analyzer， and the histopathological changes of liver cells were observed by hematoxylin-eosin （HE） staining. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect expression of long noncoding RNA-HC， and miR-130b. Real-time PCR and Western blot assay were used to detect gene and protein expression of peroxisome proliferator-activated receptor gamma （PPARγ）， liver X receptor （LXR）， ATP-binding cassette transporters A1 （ABCA1）， ATP-binding cassette transporters G1 （ABCG1）， ATP-binding cassette transporters G5 （ABCG5）， and ATP-binding cassette transporters G8 （ABCG8）. Result:Compared with the normal control group， the mice in the model group showed abnormal blood lipids， larger liver cells， obvious fat vacuoles， significantly increased expression of Lnc-HC， miR-130b in liver， and significantly decreased gene and protein expression of PPARγ， LXR， ABCA1， ABCG1， ABCG5， and ABCG8 in mice liver （P<0.05，P<0.01）. Compared with the model group， the abnormal blood lipid levels of the mice in the Xiangsha Liujunzi Tang group and the simvastatin group were improved， and the number of fatty vacuoles of liver cells was significantly reduced， the expression of liver Lnc-HC， miR-130b in Xiangsha Liujunzi Tang group decreased significantly （P<0.05，P<0.01）， the gene and protein levels of liver PPARγ， ABCA1， ABCG1， ABCG5， ABCG8 in mice of the Xiangsha Liujunzi Tang group and the simvastatin group showed an upward trend. Among them， the gene and protein expression of LXR protein in the liver of the Xiangsha Liujunzi Tang group was significantly up-regulated （P<0.05）. Conclusion:Xiangsha Liujunzi Tang may improve the lipid deposition in the liver of ApoE-/- AS mice by affecting Lnc-HC/miR-130b to regulate the cholesterol metabolism process mediated by PPARγ， thus playing a role in preventing and treating AS.
