Mechanism of Renshentang in Treatment of Atherosclerosis Based on Autophagic Effect of TRPV1 on Arterial Smooth Muscle
10.13422/j.cnki.syfjx.20230903
- VernacularTitle:基于TRPV1对动脉血管平滑肌的自噬作用探讨人参汤治疗AS的作用机制
- Author:
Yujie QI
1
;
Zhanzhan HE
1
;
Zhen YANG
2
;
Xuguang TAO
1
;
Ce CHU
1
;
Yulu YUAN
1
;
Xiangyun CHEN
2
;
Wei DING
2
;
Peizhang ZHAO
3
;
Hongxia ZHAO
1
;
Wenlai WANG
1
Author Information
1. Institute of Basic Theory of Traditional Chinese Medicine，China Academy of Chinese Medical Sciences，Beijing 100700，China
2. Beijing University of Chinese Medicine，Beijing 102488，China
3. West China Clinical Medical College，Sichuan University，Chengdu 610041，China
- Publication Type:Journal Article
- Keywords:
Renshentang recorded in Synopsis of Golden Chamber;
atherosclerosis （AS）;
transient receptor potential vanilloid subtype 1 （TRPV1）;
autophagy;
apolipoprotein E knockout （ApoE-/-） mice
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2023;29(12):55-62
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the mechanism of Renshentang， recorded in Synopsis of Golden Chamber， in the treatment of atherosclerosis （AS） based on the autophagic effect of transient receptor potential vanilloid subtype 1 （TRPV1） on arterial smooth muscle. MethodFourteen SPF-grade 8-week-old male C57BL/6J mice were assigned to the normal group and 70 8-week-old apolipoprotein E knockout （ApoE-/-） mice were assigned to the experimental group. The AS model was induced by a high-fat diet in the mice in the experimental group for eight weeks. The model mice were then randomly divided into model group， low-， medium-， and high-dose Renshentang groups （2.715， 5.43， and 10.68 g·kg-1·d-1）， and simvastatin group （0.02 g·kg-1·d-1）. Drug treatment lasted eight weeks. Serum was taken and serum total cholesterol （CHO）， triglyceride （TG）， low-density lipoprotein cholesterol （LDL-C）， and high-density lipoprotein cholesterol （HDL-C） levels were measured by assay kits to observe the changes in lipid levels in mice. The aorta was stained with hematoxylin-eosin （HE） to observe the overall pathology of the aortic root and oil red O staining was used to detect the lipid deposition in the aortic plaque and calculate the percentage of the aortic root area to the lumen area. The protein expression of TRPV1， adenylate-activated protein kinase （AMPK）， phosphorylated AMPK （p-AMPK）， autophagy effector-1 （Beclin-1）， and microtubule-associated protein 1 light chain 3 （LC3Ⅱ） in mouse aortic tissues was determined by Western blot. ResultCompared with the normal group， the model group showed increased serum CHO， TG， and LDL-C levels， decreased HDL-C， and increased aortic root plaque area （P<0.01）. Compared with the model group， the Renshentang groups showed decreased levels of CHO， TG， and LDL-C in serum （P<0.05， P<0.01）， especially in the low- and medium-dose Renshentang groups （P<0.01）. Compared with the normal group， the simvastatin group and the Renshentang groups showed reduced aortic root plaque area （P<0.05）， especially in the high-dose Renshentang group （P<0.01）. Compared with the normal group， the model group showed decreased relative expression levels of TRPV1， p-AMPK/AMPK， Beclin-1， and LC3Ⅱ/LC3Ⅰ（P<0.05， P<0.01）. Compared with the model group， the medium- and high-dose Renshentang groups showed increased relative expression levels of TRPV1， p-AMPK/AMPK， Beclin-1， and LC3Ⅱ/LC3Ⅰ（P<0.05，P<0.01）. ConclusionThe anti-AS effect of Renshentang recorded in Synopsis of Golden Chamber may be achieved by up-regulating TRPV1 expression to restore the level of autophagy mediated by AMPK.
