Study on pathophysiological mechanism underlying leptin-induced exacerbation of neuropathic pain

我们研究了脂肪细胞释放瘦素的机制，瘦素是神经病理性疼痛诱发神经病理性疼痛的媒介。结果表明，损伤周围神经组织释放高迁移率族蛋白B1 HMGB1，并作用于脂肪细胞，促进瘦素释放。已阐明HMGB1是神经病理性疼痛诱导的即刻早期介导物。

We studied the mechanism underlying leptin release from adipocytes, which is a mediator for the induction of neuropathic pain underlying of neuropathic pain. The present results indicated that HMGB1, high mobility group box 1 was released from injured peripheral nerve tissue and then, acted on adipocytes to promote leptin release. It was elucidated that HMGB1 was an immediate early mediator for induction of neuropathic pain.