电针干预慢性炎性痛的杏仁核潜在蛋白筛选

Screening of potential amygdala proteins during the intervention of chronic inflammatory pain with electroacupuncture

目的本研究旨在对完全弗氏佐剂(complete Freund’s adjuvant,CFA)诱导的慢性疼痛大鼠的杏仁核进行同位素标记的相对和绝对定量(isobaric tags for relative and absolute quantitation,iTRAQ)蛋白质组学分析,并对蛋白质表达进行综合分析,以探讨电针影响慢性疼痛的杏仁核潜在机制。方法将27只雄性SD大鼠随机分为对照组(control组)、模型组(model组)和电针组(EA组),每组9只。左后足跖掌面皮下注射100μL CFA以诱发慢性炎性痛模型。电针刺激双侧足三里、三阴交穴位共14 d。基于iTRAQ的蛋白质组学分析,研究杏仁核中的蛋白表达。结果电针可提高伤害性刺激所致炎性痛的缩足阈值(paw withdrawal thresholds,PWTs)。杏仁核中共有6319种蛋白质被定量。在这些蛋白质中,模型组相对于对照组鉴定出58种差异有显著性的蛋白质,电针组相对于对照组鉴定出37种差异有显著性的蛋白质。共有3种蛋白质在模型组和电针组的大鼠杏仁核中有显著性差异表达。结论本研究初步探讨了电针干预慢性痛的杏仁核可能机制。

Objective The current study was performed to investigate isobaric tags for relative and absolute quantitation(iTRAQ)-based quantitative proteomic analysis of the amygdala in rats with complete Freund’s adjuvant(CFA)-induced chronic pain.A comprehensive analysis of protein expression was performed to explore the underlying mechanism by which electroacupuncture(EA)affects chronic pain.Methods Twenty-seven male Sprague-Dawley(SD)rats were randomly divided into a control group(control group),model group and EA-treated group(EA group),with 9 rats in each group.Inflammatory pain was induced with an intraplantar injection of 100μL CFA into the plantar surface of the left hind paw of the male SD rats.EA stimulation of the bilateral Zusanli and Sanyinjiao acupoints was performed for 14 days.Based on iTRAQ-based proteomics analysis,we investigated protein expression in the amygdala.Results EA increased the paw withdrawal thresholds(PWTs)in rats with inflammatory pain induced by noxious stimulation.A total of 6319 proteins were quantified in the amygdala.Of these identified proteins,58 significantly altered proteins were identified in the model group compared with the con group,and 37 were identified in the EA group compared with the con group.Three proteins were found to be differentially expressed in the amygdala of model rats and EA-treated rats.Conclusions Our study confirms the possible mechanism underlying the effects of EA on the amygdala in rats with chronic pain.