Effects and mechanisms of Geniposide on rats with adjuvant arthritis

被引：78

作者：

Dai, Miao-Miao ^{[1
]}

Wu, Hong ^{[1
]}

Li, Hui ^{[1
]}

Chen, Jian ^{[1
]}

Chen, Jin-Yun ^{[1
]}

Hu, Shun-Li ^{[1
]}

Shen, Chen ^{[1
]}

机构：

[1] Anhui Univ Chinese Med, Coll Pharm, Key Lab Modernized Chinese Med Anhui Prov, Hefei 230031, Anhui, Peoples R China

来源：

INTERNATIONAL IMMUNOPHARMACOLOGY | 2014年 / 20卷 / 01期

基金：

中国国家自然科学基金;

关键词：

Adjuvant arthritis; JNK signaling; Mesenteric lymph node lymphocytes; Peripheral blood lymphocytes; Immune tolerance; Geniposide; REGULATORY T-CELLS; GROWTH-FACTOR-BETA; HEAT-SHOCK PROTEINS; N-TERMINAL KINASE; CHRONIC INFLAMMATION; RHEUMATOID-ARTHRITIS; GARDENIA-JASMINOIDES; EXPRESSION; T(H)17; INHIBITION;

D O I：

10.1016/j.intimp.2014.02.021

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Geniposide (GE), an iridoid glycoside compound, is the major active ingredient of Gardenia jasminoides Ellis (GJ) fruit which has anti-inflammatory and other important therapeutic activities. The aim of this study was to investigate the effects of GE on adjuvant arthritis (AA) rats and its possible mechanisms. AA was induced by injecting with Freund's complete adjuvant (FCA). Male SD rats were subjected to treatment with GE at 30, 60 and 120 mg/kg from days 18 to 24 after immunization. Lymphocyte proliferation was assessed by MIT. Interleukin (IL)-6, IL-17, IL-4 and transforming growth factor-beta 1 (TGF-beta(1)) were determined by ELISA. c-Jun N-terminal kinase (JNK) and phospho-JNK (p-JNK) were detected by Western blot. GE (60, 120 mg/kg) significantly relieved the secondary hind paw swelling and arthritis index, along with decreased Th17-cells cytokines and increased Treg-cell cytokines in mesenteric lymph node lymphocytes (MLNL) and peripheral blood lymphocytes (PBL) of AA rats. In addition, GE decreased the expression of p-JNK in MLNL and PBL of AA rats. In vivo study, it was also observed that GE attenuated histopathologic changes of MLN in AA rats. Collectively. GE might exert its anti-inflammatory and immunoregulatory effects through inducing Th17 cell immune tolerance and enhancing Treg cell-mediated activities by down-regulating the expression of p-JNK. The mechanisms of GE on JNK signaling in MLNL and PBL may play critical roles in the pathogenesis of rheumatoid arthritis. (C) 2014 Elsevier B.V. All rights reserved.

引用

页码：46 / 53

页数：8

共 41 条

[1] Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells [J].