Mechanisms of Renshentang in Treating AS via Regulation of Endothelial Cell Inflammation Based on TRPV1
10.13422/j.cnki.syfjx.20252201
- VernacularTitle:基于TRPV1调控内皮细胞炎症反应探讨人参汤治疗AS小鼠的作用机制
- Author:
Ce CHU
1
;
Yulu YUAN
1
;
Zhen YANG
2
;
Xuguang TAO
1
;
Xiangyun CHEN
2
;
Zhanzhan HE
3
;
Yuxin ZHANG
1
;
Yongqi XU
1
;
Wanping CHEN
1
;
Peizhang ZHAO
4
;
Wenlai WANG
1
;
Hongxia ZHAO
1
Author Information
1. Institute of Basic Theory for Chinese Medicine， China Academy of Chinese Medical Sciences， Beijing 100700， China
2. Beijing University of Chinese Medicine， Beijing 100029， China
3. Lanxi Hospital of Traditional Chinese Medicine， Jinhua 321100， China
4. West China School of Medicine， Sichuan University， Chengdu 610041， China
- Publication Type:Journal Article
- Keywords:
Renshentang;
atherosclerosis;
transient receptor potential vanilloid subtype 1;
endothelial cells;
inflammation
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(6):46-53
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the mechanisms by which Renshentang treats atherosclerosis （AS） in mice， focusing on the regulation of endothelial inflammatory responses mediated by transient receptor potential vanilloid subtype 1 （TRPV1）. MethodsAn AS model was established in apolipoprotein E knockout （ApoE-/-） mice fed a high-fat diet. The mice were randomly divided into a simvastatin group （0.02 g·kg-1·d-1） and low-， medium-， and high-dose Renshentang groups （1.77， 3.54， 7.08 g·kg-1·d-1）， with 12 mice in each group. ApoE-/- mice were fed a high-fat diet and treated simultaneously. C57BL/6J mice fed a normal diet served as the normal group （n=9）. After continuous administration for 12 weeks， mice were anesthetized and the aortas were collected. Oil Red O staining was used to observe lipid plaque formation in the aorta. Hematoxylin-eosin （HE） staining was performed to examine pathological changes in the aortic root. Immunohistochemistry was used to analyze the levels of pro-inflammatory factors tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β）， as well as the expression of TRPV1， phosphorylated phosphoinositide 3-kinase （p-PI3K）， and phosphorylated protein kinase B （p-Akt） in the aortic root. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect endothelial nitric oxide synthase （eNOS） mRNA expression in the aorta， and Western blot was used to detect TRPV1 protein expression. ResultsCompared with the normal group， the model group showed a significant increase in aortic plaque formation （P<0.01） and significantly elevated levels of TNF-α and IL-1β in the aortic root （P<0.01）. The expression levels of TRPV1， p-PI3K， and p-Akt were decreased （P<0.05， P<0.01）， and eNOS mRNA expression was reduced （P<0.05， P<0.01）. Compared with the model group， all Renshentang groups significantly reduced aortic plaque formation （P<0.01）， significantly decreased TNF-α and IL-1β levels （P<0.01）， and markedly increased the expression levels of TRPV1， p-PI3K， p-Akt， and eNOS mRNA （P<0.05， P<0.01）. ConclusionRenshentang may inhibit endothelial inflammation and suppress the formation of AS by increasing TRPV1 protein expression and up-regulating the PI3K/Akt/eNOS signaling pathway， which may be one of the molecular mechanisms underlying its therapeutic effect against AS.
