Paeoniflorin-6′-O-benzene sulfonate ameliorates progression of adjuvant-induced arthritis by inhibiting interaction between Ahr and GRK2 of fibroblast-like synoviocytes  

作　　者：ZHANG Bin-jie WANG Yue-ye JIA Cheng-yan LI Su-su WANG Xin-wei XU Yuan CHEN A-yuan XU He-peng WANG Chun WEI Wei CHANG Yan 

机构地区：[1]Key Laboratory of Anti-Inflammatory and Immune Medicine,Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine,Institute of Clinical Pharmacology,Anhui Medical University,Ministry of Education,Hefei 230032,China

出　　处：《中国药理学与毒理学杂志》2021年第10期777-777,共1页Chinese Journal of Pharmacology and Toxicology

基　　金：National Nature Science Foundation of China(81573443,82173824,81973332);Anhui Province Natural Science Fund(170808J10);Anhui Provincial Natural Science Foundation(2108085MH320);and Collaborative Innovation Project of Key Scientific Research Platform in Anhui Universities(GXXT-2020-065)。

摘　　要：OBJECTIVE Aryl hydrocarbon receptor(Ahr)is thought to be a crucial factor that regulates immune responses,which may be involved in the pathogenesis of autoimmune inflammation including rheumatoid arthritis(RA).The results of our group in recent years have shown that CP-25,a novel ester derivative of paeoniflorin,has a good effect on improving RA animal models.However,whether the anti-arthritis effect of CP-25 is related to Ahr remains unclear.METHODS CP-25 treatment ameliorated adjuvant-induced arthritis(AA),a mouse model of RA,by inhibiting Ahr-related activities in fibroblasts like synoviocytes(FLS).AA rats were treated with CP-25 or paroxetine from day 17 to 33 after immunization.RESULTS CP-25 alleviated arthritis symptoms and the pathological changes,decreased the expression of Ahr in the synovium and FLS of AA rats.Besides,treatment with CP-25 reduced the proliferation and migration of MH7A caused by Ahr activation.In addition,we also demonstrated that CP-25 down-regulated the co-expression and co-localization of Ahr and G protein-coupled receptor kinase 2(GRK2)in MH7A.CONCLUSION The data presented here demonstrated that CP-25 suppressed FLS dysfunction in rats with AA,which were associated with reduced Ahr activation and the interaction between Ahr and GRK2.

关 键 词：aryl hydrocarbon receptor G protein-coupled receptor kinase 2 rheumatoid arthritis CP-25 fibroblasts like synoviocyte adjuvant-induced arthritis 

分 类 号：R285[医药卫生—中药学]