摘要
目的:探讨热休克蛋白(Hsp)72对类风湿关节炎患者滑膜细胞IL-6、IL-8表达的影响,从NFκ-B信号通路活化的角度阐明其作用机制。方法:原代培养类风湿关节炎患者的滑膜细胞;采用酶联免疫吸附试验(ELISA)法检测细胞培养上清中IL-6和IL-8的含量;采用Western blot检测滑膜细胞NFκ-B和ΙκBα蛋白的表达变化;采用免疫荧光技术检测NFκ-B核移位的变化。结果:Hsp72抑制TNFα-所诱导的IL-6和IL-8的生成;Hsp72抑制TNFα-所诱导NFκ-B在核内的表达和移位;Hsp72抑制TNFα-所诱导ΙκBα蛋白降解。结论:Hsp72可能通过抑制滑膜细胞IL-6、IL-8表达及抑制NF-κB信号通路活化而对类风湿关节炎发挥抗炎作用。
Objective： To investigate the effects of heat shock protein 72 （Hsp72） on the expression of IL-6 and IL-8 and activation of NF-κB in synoviocytes from patients suffered from rheumatoid arthritis （RA）. Methods： IL-6 and IL-8 concentrations in culture supematants were measured using enzyme-linked immunosorbent assays （ELISA）. Nuclear translocation of NF-κB and degradation of the inhibitory protein IκBa were examined using immunohistochemistry and Western blot. Results： Hsp72 down-regulated IL-6 and IL-8 production in RA synoviocytes induced by tumor necrosis factor-α（TNF-α）. Hsp72 inhibited nuclear translocation of NF-κB and degradation of of induced by TNF-α. Conclusion： Hsp72 has an antinflammatory effect on RA by down-regulation of IL-6 and IL-8 in synoviocytes, which is mediated through inhibiting the activation of NF-κB signal pathways.
出处
《中国应用生理学杂志》
CAS
CSCD
2012年第4期336-339,共4页
Chinese Journal of Applied Physiology
基金
浙江省自然科学基金资助(Y2090233)
