The effect of taurochenodeoxycholic acid on the glucocorticoid receptor-mediated PLC-IP3-calcium pathway in synoviocytes derived from a rat adjuvant arthritis model
文献类型: 外文期刊
作者: Wu, Jindi 2 ; Bai, Fan 4 ; Guanqia, Sangjide 1 ; Li, Peifeng 1 ; Cao, Jinshan 1 ; Qian, Yinghong 4 ; Mao, Wei 1 ;
作者机构: 1.Inner Mongolia Agr Univ, Coll Vet Med, Lab Vet Pharmacol, Hohhot, Peoples R China
2.Engn Inner Mongolia Agr Univ, Coll Food Sience, Hohhot, Peoples R China
3.Inner Mongolia Agr Univ, Key Lab Clin Diag & Treatment Tech Anim Dis, Minist Agr, Hohhot, Peoples R China
4.Inner Mongolia Acad Agr & Anim Husb Sci, Hohhot, Peoples R China
5.Inner Mongolia Acad Agr & Anim Husb Sci, Hohhot 010031, Peoples R China
关键词: taurochenodeoxycholic acid; rat adjuvant arthritis model; glucocorticoid receptor; phospholipase C-inositol trisphosphate-Ca2+ signalling pathway
期刊名称:VETERINARSKI ARHIV ( 影响因子:0.5; 五年影响因子:0.6 )
ISSN: 0372-5480
年卷期: 2024 年 94 卷 1 期
页码:
收录情况: SCI
摘要: Taurochenodeoxycholic acid is one of the main active components of the bile acid pool and has important anti-inflammatory and immunomodulatory properties. This study aimed to explore the therapeutic effects and mechanism of action of taurochenodeoxycholic acid in inflammatory arthritis using a rat adjuvant arthritis model. Fibroblast-like synoviocytes were derived from rats with adjuvant arthritis and cultured using the adherent tissue explant method. Western blotting, enzyme-linked immunosorbent assay, and fluorescent probe-based methods were used to detect the effects of taurochenodeoxycholic acid on glucocorticoid receptor expression, phospholipase C protein levels, and inositol trisphosphate and intracellular free Ca2+ concentrations in primary rat fibroblast-like synoviocytes. Taurochenodeoxycholic acid significantly induced the expression of glucocorticoid receptor (P<0.05) and phospholipase C (P<0.05) and enhanced phospholipase C phosphorylation. Moreover, taurochenodeoxycholic acid significantly increased the levels of inositol trisphosphate (P<0.05) and intracellular free Ca2+ concentrations. Our results suggest that taurochenodeoxycholic acid activates the phospholipase C-inositol trisphosphate-Ca2+ signalling pathway by increasing glucocorticoid receptor expression. These findings provide a theoretical foundation for future studies on the molecular mechanisms underlying taurochenodeoxycholic acid-based treatment of adjuvant arthritis. In conclusion, taurochenodeoxycholic acid exerted anti-inflammatory and immunomodulatory effects by enhancing glucocorticoid receptor expression via non-genomic signalling.
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