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HMGB1-TLR4-NF-κB信号转导与糖尿病神经病理性疼痛关系的研究进展

来自:中国糖尿病杂志  编辑:袁超 曹红|点击数:|2014-08-28

·文献综述·

  【摘要】 正常生理状态下,高迁移率族蛋白1(HMGB1)存在于核内,稳定核染色体和调控蛋白转录、翻译,但当病理状态时,HMGB1转移到胞浆,与Toll样受体(TLRs)结合,促使核转录因子κB(NF-κB)分子活化,引起细胞因子释放。TLRs是抵抗病原菌对宿主入侵的主要识别和信号传递受体,在中枢、外周神经系统中都有表达,对糖尿病神经病理性疼痛(DNP)的产生具有重要意义。

  【关键字】 糖尿病神经病理性疼痛;高迁移率族蛋白1;Toll样受体;核转录因子κB

  【Summary】 In normal physiological condition, high mobility group box-1 protein (HMGB1) stays in nuclear, stabling nucleus chromosome and controlling the chromosome transcription and translation. But when the cells are in the pathological state, a variety of activated HMGB1 are released out from nuclear. The intracellular HMGB1 combines with its receptor TLRs, activating the NF-κB molecules, which transfers into the nuclear and causes cytokines released. TLRs are the main recognition and signal transfer receptors in resisting the invasion of the pathogenic. TLRs are expressed in the central and peripheral nervous system. And they have an important role for the diabetes neuropathic pain (DNP).

  【Key words】 Diabetes neuropathic pain (DNP);HMGB1;TLRs;NF-κB

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