Zhang Jingyue, Sun Juan, Chen Dezhi, Kang Jiyu, Peng Chuan, Chang Xiaotao, Zhou Huacheng
Department of Pain Management, the Fourth Affiliated Hospital of Harbin Medical University, No.37, Yiyuan Street, Nangang District, Harbin, Heilongjiang Province, 150001, China.
Department of Pain Management, the First Affiliated Hospital of Harbin Medical University, No.25 Post Office Street, Nangang District, Harbin, Heilongjiang Province, 150001, China.
Lasers Med Sci. 2023 Jan 31;38(1):58. doi: 10.1007/s10103-023-03717-1.
Intervertebral disc degeneration (IVDD) mainly manifests as an imbalance between the synthesis and degradation of cellular and extracellular matrix (ECM) components. The cytokine interleukin (IL)-1β-induced inflammatory response of intervertebral discs causes ECM degradation. The aim of this study was to investigate the effects of a 970-nm diode laser therapy (DLT) on inflammatory cytokine IL-1β and ECM degradation proteinases in nucleus pulposus (NP) tissues in a puncture-induced rabbit IVDD model. Thirty-six New Zealand white rabbits were randomly divided into six groups: the normal group, IVDD group, laser group, sham laser group, IVDD + anisomycin (p38MAPK signaling pathway agonist), and laser + anisomycin group. Effects of laser on IVDD progression were detected using radiographic and magnetic resonance imaging. Hematoxylin and eosin, Alcian blue, safranin O-fast green staining, western blotting, and immunohistochemistry staining were performed for the histological analysis and molecular mechanism underlying protection against puncture-induced matrix degradation in NP tissues by DLT. DLT reduced the degree of disc degeneration in the gross anatomy of the disc and increased the T2-weighted signal intensity of NP. Inflammatory cytokine IL-1β levels in the disc were significantly reduced after DLT suppressed the matrix-degrading proteinases MMP13 and ADAMTS-5 and upregulated the protein expression of collagen II and aggrecan. Moreover, it inhibited the p38MAPK signaling pathway in NP tissues in a puncture-induced rabbit IVDD model. DLT reduced puncture-induced overexpression of inflammatory cytokines, mainly IL-1β, thus inhibiting matrix degeneration of NP tissues and ameliorating IVDD. This may be related to inhibition of the p38 MAPK signaling pathway.
椎间盘退变（IVDD）主要表现为细胞和细胞外基质（ECM）成分合成与降解之间的失衡。细胞因子白细胞介素（IL）-1β诱导的椎间盘炎症反应会导致ECM降解。本研究的目的是在穿刺诱导的兔IVDD模型中，研究970纳米二极管激光疗法（DLT）对髓核（NP）组织中炎性细胞因子IL-1β和ECM降解蛋白酶的影响。将36只新西兰白兔随机分为六组：正常组、IVDD组、激光组、假激光组、IVDD +茴香霉素（p38丝裂原活化蛋白激酶信号通路激动剂）组和激光+茴香霉素组。使用X线摄影和磁共振成像检测激光对IVDD进展的影响。进行苏木精和伊红染色、阿尔辛蓝染色、番红O-固绿染色、蛋白质印迹法和免疫组织化学染色，以分析组织学并探究DLT对穿刺诱导的NP组织基质降解的保护作用的分子机制。DLT降低了椎间盘大体解剖中的退变程度，并增加了NP的T2加权信号强度。DLT抑制基质降解蛋白酶MMP13和ADAMTS-5并上调胶原蛋白II和聚集蛋白聚糖的蛋白表达后，椎间盘内炎性细胞因子IL-1β水平显著降低。此外，在穿刺诱导的兔IVDD模型中，它抑制了NP组织中的p38丝裂原活化蛋白激酶信号通路。DLT减少了穿刺诱导的炎性细胞因子（主要是IL-1β）的过度表达，从而抑制了NP组织的基质退变并改善了IVDD。这可能与抑制p38丝裂原活化蛋白激酶信号通路有关。
