文章摘要

HSF-1在HMGB1诱导的炎症反应中的作用

作者: 1尹朝奇, 1贺全勇, 1罗成群, 1周建大, 1陈佳, 1李萍, 1朱颉, 1彭浩, 1徐阳成, 1陶如意
1 中南大学湘雅三医院 烧伤整形科，湖南 长沙 410013
通讯: 尹朝奇 Email: yinchaoqi@163.com
DOI: 10.3978/.10.3978/j.issn.1005-6947.2016.09.011
基金: 湖南省卫生厅科研基金资助项目, B2012-030

摘要

目的：探讨热休克转录因子1（HSF-1）在高迁移率族蛋白1（HMGB1）所诱导的炎症反应中的作用。方法：不同浓度HMGB1作用于RAW264.7细胞不同时间后，用ELISA法检测细胞上清液TNF-α水平；分别用免疫荧光法与Western blot法检测HMGB1作用后，RAW264.7细胞NF-κB核转移情况与HSF-1表达。观察干扰HSF-1表达后，HMGB1诱导RAW264.7细胞TNF-α表达的变化。结果：HMGB1作用后，RAW264.7细胞分别在4、12 h出现两次TNF-α分泌高峰，且TNF-α的释放量随HMGB1浓度的增加而增加。HMGB1作用后，RAW264.7细胞的NF-κB核转移明显增强，HSF-1表达明显增加（均P<0.05）。干扰HSF-1表达后，HMGB1诱导RAW264.7细胞产生的TNF-α量较未干扰的RAW264.7细胞明显增加（P<0.05）。结论：HMGB1能诱导RAW264.7细胞的炎症反应与HSF-1的表达，但HSF-1可能对HMGB1诱导的炎症反应有负反馈性抑制作用。
关键词： 胰腺炎，急性坏死性 全身炎症反应综合征 高迁移率族蛋白质类 热休克转录因子1

Role of HSF-1 in inflammatory response induced by HMGB1

Authors: 1YIN Chaoqi, 1HE Quanyong, 1LUO Chengqun, 1ZHOU Jianda, 1CHEN Jia, 1LI Ping, 1ZHU Jie, 1PENG Hao, 1XU Yangcheng, 1TAO Ruyi
1 Department of Burns and Plastic Surgery, the Third Xiangya Hospital, Central South University, Changsha 410013, China

CorrespondingAuthor:YIN Chaoqi Email: yinchaoqi@163.com

Abstract

Objective: To investigate the role of heat shock transcription factor 1 (HSF1) in inflammatory response induced by high mobility group protein B1 (HMGB1). Methods: The TNF-α contents in the supernatants of RAW264.7 cells after exposure to different concentrations of HMGB1 for different times were determined by ELISA assay. The NF-κB nuclear translocation and HSF-1 expression in RAW264.7 cells after HMGB1 treatment were examined by immunofluorescence and Western blot, respectively. The change in TNF-α expression induced by HMGB1 in RAW264.7 cells after interference of HSF-1 expression was observed. Results: RAW264.7 cells presented two peaks of TNF-α release at 4 and 12 h respectively after HMGB1 treatment, and the TNF-α release level was increased with the elevation of HMGB1 concentration. The NF-κB nuclear translocation was significantly enhanced and HSF-1 expression was significantly increased in RAW264.7 cells after HMGB1 treatment (both P<0.05). The TNF-α expression induced by HMGB1 in RAW264.7 cells after interference of HSF-1 expression was significantly increased compared with RAW264.7 cells without HSF-1 interference (P<0.05). Conclusion: HMGB1 can induce inflammatory response and HSF-1 expression in RAW264.7 cells, but HSF-1 may play a negative feedback inhibitory role in the HMGB1-induced inflammation.
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