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艾灸治疗慢性炎性内脏痛的机制研究:脊髓p38 MAPK/ELK1信号通路的调节
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艾灸治疗慢性炎性内脏痛的机制研究:脊髓p38 MAPK/ELK1信号通路的调节
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Journal Article
艾灸治疗慢性炎性内脏痛的机制研究:脊髓p38 MAPK/ELK1信号通路的调节
2024
Overview
R2-03; 目的:从调节脊髓p38丝裂原活化蛋白激酶(MAPK)/Ets样转录因子1(ELK1)信号通路角度,探讨艾灸治疗慢性炎性内脏痛(CIVP)的中枢机制及其镇痛效应.方法:清洁级雄性Sprague-Dawley大鼠随机分为正常组、模型组、隔药灸组、假隔药灸组、p38 MAPK抑制剂组和二甲基亚砜(DMSO)组.采用2,4,6-三硝基苯磺酸合50%乙醇灌肠制备CIVP大鼠模型.隔药灸组给予隔附子饼灸治疗;假隔药灸组处理同隔药灸组,但不点燃艾炷;p38 MAPK抑制剂组在大鼠L5-L6间鞘内注射SB203580;DMSO组在L5-L6间鞘内注射2%DMSO.通过腹壁撤回反射(AWR)评分、机械刺激缩足阈值(MWT)及热缩足潜伏期(TWL)观察各组大鼠痛行为变化;应用苏木素-伊红染色镜下观察各组大鼠结肠组织形态学变化;采用免疫印迹法和实时荧光定量聚合酶链反应检测各组大鼠脊髓凋亡信号调节激酶1(ASK1)、MAPK激酶(MKK)3/6、p38 MAPK、ELK1和丝裂原应激活化蛋白激酶1(MSK1)磷酸化蛋白和mRNA的表达.结果:与正常组比较,CIVP大鼠结肠炎性损伤严重,病理损伤评分明显升高;不同压力结直肠扩张(CRD)刺激下AWR评分均增加,MWT及TWL均降低;脊髓p38 MAPK、ELK1、MSK1、ASK1、MKK3/6磷酸化蛋白和mRNA表达显著增加(P<0.01).经隔药灸治疗后,大鼠结肠损伤有所修复,病理损伤评分降低;不同压力CRD刺激下,AWR评分均减少,MWT、TWL升高;脊髓p38 MAPK、ELK1、ASK1、MKK3磷酸化蛋白和mRNA表达降低,与模型组、假隔药灸组比较,差异均有统计学意义(P<0.01).隔药灸组与p38 MAPK抑制剂组相比、DMSO组与模型组相比,上述指标均无显著差异(P>0.05).结论:隔药灸能通过下调CIVP大鼠脊髓ASK1、MKK3、p38 MAPK、ELK1磷酸化蛋白和mRNA的表达发挥镇痛效应.抑制脊髓p38 MAPK/ELK1信号通路活化可能是隔药灸缓解疼痛,治疗CIVP的机制之一.
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