Effect of Huangqi San on AMPK/ACC/CPT1 pathway in hyperlipidemia rats.
10.19540/j.cnki.cjcmm.2018.0082
- Author:
Meng-Jiao HAO
1
;
Yuan-Xia DANG
2
;
Xin-Xin ZHOU
2
;
Chun-Yi WANG
2
;
Ying GAO
1
;
Wei-Min LI
2
Author Information
1. Mathematical Engineering Academy of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou 510006, China.
2. School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou 510006, China.
- Publication Type:Journal Article
- Keywords:
AMP protein kinase;
HMG-CoA reductase;
Huangqi San;
acetyl-CoA carboxylase;
hyperlipidemia
- From:
China Journal of Chinese Materia Medica
2018;43(12):2586-2592
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the mechanism of the treatment of hyperlipidemia rats induced by Huangqi San. The 40 male SD rats were randomly divided into normal group, model group, Huangqi San low and high dose group (1, 2 g·kg⁻¹), and positive lipitor group (2 mg·kg⁻¹). The normal group feeds on base feed, and other groups feed on high-fat feed. After 8 weeks, the hyperlipidemia model was successful. After intervention by drugs for 13 weeks, fasting blood glucose, total cholesterol, triglycerides and LDL cholesterol content of all rats were measured. The pathological changes of liver and skeletal muscle of rats were observed in rats. Real-time PCR and Western blot were used to detect the mRNA and protein expression levels of AMPK signaling pathway in the liver and skeletal muscles (AMPK, ACC, CPT1A, SREBP2, HMGCR). The degree of FPG, TC, TG and LDL-C were the highest in the model group, and the liver and skeletal muscle pathology were the most obvious. After intervention by Huangqi San and lipitor, a significant reduction in the blood sugar blood fat, liver, and skeletal muscle injury has improved significantly, except SREBF2 and HMGCR mRNA and protein expression of this enzyme is reduced, other AMPK pathway related mRNA and protein expression increased significantly. Huangqi San effect is superior to lipitor. Huangqi San may improve hyperlipidemia by regulating the AMPK signaling pathway, increasing the oxidation of fatty acids and inhibiting cholesterol synthesis.
