烙灸疗法介导Fas/FasL信号通路对髓核细胞外基质环境的影响

Effect of Nucleus Pulposus Extracellular Matrix Environment through Fas/FasL Signaling Pathway Mediated by Cautery Moxibustion

目的探讨烙灸疗法介导Fas/FasL信号通路对腰椎间盘突出症髓核细胞外基质环境的调控机制。方法将120只雄性SD大鼠随机分为烙灸组、拮抗剂组、模型对照组、空白对照组。除空白对照组30只大鼠外均采用针刺手术方法制作大鼠腰椎间盘突出后髓核重吸收模型,烙灸组和拮抗剂组的大鼠在造模后1个月进行干预,分为3批,每批10只,分别在干预1、3、6个月后进行取材;其余2组不予干预,在造模后分3批进行取材。结果模型对照组、拮抗剂组与烙灸组的髓核细胞凋亡指数明显高于空白对照组(P<0.05),而烙灸组的髓核细胞凋亡指数高于模型对照组及拮抗剂组(P<0.05);烙灸组髓核细胞外基质中的MMP-1、MMP-2、MMP-3、MMP-13和ADAMTS-4mRNA表达水平高于模型对照组、拮抗剂组(P<0.05)。烙灸组髓核细胞外基质MMP-1、MMP-2、MMP-3、MMP-13蛋白表达量高于模型对照组、拮抗剂组及空白对照组(P<0.05);烙灸组髓核细胞外基质中的ADAMTS-4蛋白表达较模型对照组、拮抗剂组明显增高(P<0.01)。结论烙灸疗法通过Fas/FasL信号通路的介导,可提高MMPs和ADAMTS-4表达,从而加速细胞外基质的降解,促进腰椎间盘突出后髓核重吸收。

Objective To investigate the regulation mechanism of the Fas/FasL signaling pathway mediated by cautery moxibustion therapy on the extracellular matrix environment of the nucleus pulposus.Methods 120 male SD rats were randomly divided into a cautery moxibustion group,an antagonist group,a model control group,and a blank control group.Except for the 30 rats in the blank control group,acupuncture surgery was used to make rat lumbar disc herniated nucleus pulposus reabsorption models.The rats in the cautery group and the antagonist group were intervened one month after modeling.Three batches of 10 animals were collected after the intervention for January,March,and June respectively;the other two groups were not interfered,and the samples were collected in three batches after the model was built.Results The number of Fas1 positive cells in the cautery moxibustion group was significantly higher than that of the model control group(P<0.05),and the protein expressions of MMP-1,MMP-2,MMP-3,MMP-13,IL-1,and ADAMTS-4 were significantly lower than those of the model control group.The model control group and the antagonist group(P<0.05),and there is no significant difference between the model control group and the antagonist group.Conclusion Cautery moxibustion therapy can increase the expression of MMPs and ADAMTS-4 through Fas/FasL signaling pathway,thereby accelerating the degradation of extracellular matrix and promoting the reabsorption of nucleus pulposus after lumbar disc herniation.