慢性术后疼痛（chronic post-surgical pain syndrome，CPSP）是临床常见的难题且机制不明。 已有研究表明围手术期患者的心理及躯体应激能导致CPSP的发生，但具体机制不明。前期预实验显示，围手术期应激可延迟术后切口痛恢复且导致去甲基化酶TET1的下降，目前尚无相关文献报导。本研究以围手术期心理精神因素对慢性疼痛的转归为背景，采用睡眠剥夺机制制作急性疼痛向慢性疼痛转变的动物模型（申请人已发表），利用 Elisa、 qPCR、 Western-blot、CHIP、SiRNA干扰、HSV病毒包装克隆TET1全CDS、神经节显微注射、鞘内置管给药、原代神经元细胞的培养、双荧光素酶报告基因、单细胞PCR、免疫荧光、CPP、电生理、DNA Dot blotting、TAB-Seq等实验方法，探索TET1参与术后慢性疼痛发生的机制，对更全面阐明表观遗传参与疼痛调控提供理论

Chronic postoperative pain (CPSP) is a common clinical problem, however, little is known about the mechanism. Though it has been revealed that perioperative stress caused the CPSP, the underlying mechanism remain unclear. The preliminary experiments suggest that perioperative stress do delay the pain recovery time, moreover, the demethylation enzyme TET1 expression decreased and MOR expression increased were found in postoperative incision pain rat, which hasn’t been reported by now. Applied to the sleep deprivation incision pain model(have been published by applicant) , this study using Elisa, qPCR, Western blot, CHIP, SiRNA, HSV-TET1 overexpression, ganglion microinjection, intrathecal injection, DRG cell culture, dual luciferase report, single-cell PCR, immunofluorescence staining, CPP, electrophysiology, DNA Dot blotting and TAB-Seq experimental methods, to explore the mechanism of TET1 invoved in postoperative chronic pain, thus illuminating the participation of epigenetic mechanism in chronic pain and providing a new idea for chronic pain treatment.