| 闫悦,阿日嘎太,闫金玉,赵小娟,张佳林.低强度激光联合超短波改善大鼠腰椎间盘退变的分子机制研究[J].中国康复,2026,41(7):387-394 |
| 低强度激光联合超短波改善大鼠腰椎间盘退变的分子机制研究 |
| Low-level laser therapy combined with ultrashort wave ameliorates lumbar intervertebral disc degeneration in rats by regulating the p38 MAPK signaling pathway |
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| DOI：10.3870/zgkf.2026.07.001 |
| 中文关键词: 低强度激光 超短波 腰椎间盘退变 p38丝裂原活化蛋白激酶 炎症因子 |
| 英文关键词: low-level laser therapy ultrashort wave lumbar intervertebral disc degeneration p38 mitogen-activated protein kinase inflammatory cytokine |
| 基金项目:内蒙古医学科学院公立医院科研联合基金科技项目（2025GLLH0228）；内蒙古自治区首府地区公立医院高水平临床专科建设科技项目（2024SGGZ090）；内蒙古医科大学“善学”人才项目（ZY20242142） |
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| 中文摘要: |
| 目的：探讨低强度激光（LLLT）联合超短波（USW）对腰椎间盘退变（LIDD）模型大鼠的作用，并基于p38丝裂原活化蛋白激酶（p38 MAPK）信号通路分析其相关分子机制。方法：将40只SD大鼠随机分为空白对照组（C组）、模型对照组（MC组）、USW治疗组（U组）、LLLT治疗组（L组）、LLLT联合USW治疗组（LU组），每组8只。MC组、U组、L组、LU组均采用纤维环（AF）穿刺法构建LIDD模型，按组别给予相应的干预4周。4周后，采用苏木精-伊红（HE）染色观察大鼠椎间盘组织形态学改变。采用酶联免疫吸附试验（ELISA）检测大鼠血清肿瘤坏死因子-α（TNF-α）与白细胞介素-1β（IL-1β）水平。采用蛋白质免疫印迹法（WB）检测大鼠椎间盘组织p38 MAPK、磷酸化p38丝裂原活化蛋白激酶（p-p38 MAPK）、丝裂原活化蛋白激酶激活蛋白激酶2（MK2）及激活转录因子-2（ATF-2）表达水平。采用实时荧光定量逆转录聚合酶链反应（RT-qPCR）检测大鼠椎间盘组织中基质金属蛋白酶-3（MMP-3）、基质金属蛋白酶-9（MMP-9）mRNA水平。结果：4组大鼠LIDD模型成功建立。干预4周后，与MC组比较，U组、L组、LU组大鼠椎间盘组织形态结构均改善，其中LU组修复效果最佳。与C组比较，MC组血清IL-1β、TNF-α水平及椎间盘组织p-p38 MAPK、MK2、ATF-2蛋白表达均升高（P＜0.01），MC组MMP-3、MMP-9 mRNA表达亦升高（P＜0.01）；与MC组比较，各治疗组（L、U、LU组）上述血清炎症指标及通路蛋白均降低（P＜0.05），LU组MMP-3、MMP-9 mRNA表达亦降低（P＜0.01）。治疗组间比较，LU组血清IL-1β、TNF-α和椎间盘p-p38 MAPK、MK2、ATF-2及MMP-3 mRNA表达均低于U组（P＜0.05），其血清炎症指标、ATF-2、MMP-3 mRNA表达与L组比较差异无统计学意义，而p-p38 MAPK、MK2蛋白表达低于L组（P＜0.05）。5组p38 MAPK总蛋白表达无明显差异。结论：低强度激光联合超短波可能通过抑制p38 MAPK信号通路活化调节LIDD模型大鼠炎症微环境，从而对LIDD治疗发挥积极作用。 |
| 英文摘要: |
| Objective: To investigate the effects of low-level laser therapy (LLLT) combined with ultrashort wave (USW) on a rat model of lumbar intervertebral disc degeneration (LIDD) and to explore its potential mechanisms based on the p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway. Methods: Totally, 40 SD male rats were randomly divided into 5 groups: blank control (C group), model control (MC group), USW therapy (U group), LLLT (L group), and combined treatment (LU group) (n=8 per group). The LIDD model was established in the MC, U, L and LU groups using the annulus fibrosus (AF) puncture method, and the corresponding interventions were administered for 4 weeks according to the different groups. After 4 weeks, haematoxylin and eosin (HE) staining was used to observe morphological changes in the rat intervertebral disc tis-sue. Enzyme-linked immunosorbent assay (ELISA) was employed to measure serum levels of tumour necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in rats. Western blot (WB) was used to detect the expression levels of p38 MAPK, phosphorylated p38 MAPK (p-p38 MAPK), mitogen-activated protein kinase 2 (MK2) and activator of transcription factor-2 (ATF-2) in rat intervertebral disc tissue. Real-time reverse transcription polymerase chain reaction (RT-qPCR) was used to detect the mRNA levels of matrix metalloproteinase-3 (MMP-3) and MMP-9 in rat intervertebral disc tissue. Results: LIDD models were successfully established in 4 groups of rats. After 4 weeks of intervention, compared with the MC group, the morphological structure of the intervertebral disc tissue was improved in the U, L and LU groups, with the LU group showing the best repair outcome. Compared with C group, serum IL-1β and TNF-α levels, as well as the expression of p-p38 MAPK, MK2 and ATF-2 proteins in the intervertebral disc, were all elevated in the MC group (P<0.01); the expression of MMP-3 and MMP-9 mRNA was also elevated in the MC group (P<0.01). Compared with the MC group, the aforementioned serum inflammatory markers and pathway proteins were reduced in all treatment groups (P<0.05), and the expression of MMP-3 and MMP-9 mRNA was also reduced in the LU group (P<0.01). In comparisons between treatment groups, serum IL-1β and TNF-α levels, as well as disc p-p38 MAPK, MK2, ATF-2 and MMP-3 mRNA expression, were all lower in the LU group than in the U group (P<0.05). The serum inflammatory markers, ATF-2, MMP-3 mRNA expression in the LU group showed no statistically significant differences compared with the L group, whilst p-p38 MAPK and MK2 protein expression was lower in the LU group than in the L group (P<0.05). There were no significant differences in total p38 MAPK protein expression across the five groups.Conclusion: LLLT combined with USW may play a positive role in the treatment of LIDD by regulating the inflammatory microenvironment in rats with an LIDD model through the inhibition of p38 MAPK signaling pathway. |
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