[热休克蛋白72对类风湿关节炎滑膜细胞中白细胞介素-6、白细胞介素-8表达及核因子-κB激活的影响]
[The effect of Hsp72 on IL-6, IL-8 expression and activation of NF-kappaB in synoviocytes of rheumatoid arthritis].
作者信息
Luo Xin-Jing, Mo Xuan-Rong, Zhou Ling-Ling
机构信息
Department of Physiology, Medical College of Taizhou University, Taizhou 318000, China
出版信息
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2012 Jul;28(4):336-9.
OBJECTIVE
To investigate the effects of heat shock protein 72 (Hsp72) on the expression of IL-6 and IL-8 and activation of NF-kappaB in synoviocytes from patients suffered from rheumatoid arthritis (RA).
METHODS
IL6 and IL8 concentrations in culture supernatants were measured using enzyme-linked immunosorbent assays (ELISA). Nuclear translocation of NF-kappaB and degradation of the inhibitory protein IkappaBalpha 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-alpha (TNF-alpha). Hsp72 inhibited nuclear translocation of NF-kappaB and degradation of IkappaBalpha induced by TNF-alpha.
CONCLUSION
Hsp72 has an anti-inflammatory effect on RA by down-regulation of IL-6 and IL-8 in synoviocytes, which is mediated through inhibiting the activation of NF-KalphaB signal pathways.
目的
研究热休克蛋白72（Hsp72）对类风湿关节炎（RA）患者滑膜细胞中白细胞介素-6（IL-6）和白细胞介素-8（IL-8）表达及核因子κB（NF-κB）激活的影响。
方法
采用酶联免疫吸附测定（ELISA）法检测培养上清液中IL-6和IL-8的浓度。采用免疫组织化学和蛋白质印迹法检测NF-κB的核转位及抑制蛋白IκBα的降解情况。
结果
Hsp72可下调肿瘤坏死因子-α（TNF-α）诱导的RA滑膜细胞中IL-6和IL-8的产生。Hsp72可抑制TNF-α诱导的NF-κB核转位及IκBα降解。
结论
Hsp72通过下调滑膜细胞中IL-6和IL-8对RA具有抗炎作用，这是通过抑制NF-κB信号通路的激活介导的。
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