银质针导热疗法对肌筋膜疼痛综合征大鼠海马神经可塑性的影响

Effects of Silver-Needle Conductive Heat Therapy on Hippocampal Neuroplasticity in Rats with Myofascial Pain Syndrome

摘要:

目的：观察银质针导热疗法对肌筋膜疼痛综合征大鼠海马神经元及突触可塑性的影响，探讨其在中枢层面改善慢性疼痛状态的可能机制。方法：20只雄性SD大鼠采用随机数字表法分为正常组，模型组，银质针导热组，每组6只。对右股内侧肌击打和离心运动复制MPS模型。在造模前1天（T0）、造模第4周（T1）、造模第8周（T2）、银质针导热治疗后第2周（T3）分别检测机械刺激缩足阈值（mechanical withdrawal threshold，MWT）和热缩足潜伏期（thermal withdrawal latency，TWL）；检测大鼠右侧股内侧肌肌电图电活动；苏木精-伊红染色及尼氏染色染色观察大鼠海马齿状回神经元形态；透射电镜观察大鼠海马突触超微结构；免疫印迹法检测PSD-95、Syn蛋白表达。结果：与正常组相比，模型组MWT及TWL明显降低(P < 0.01)；经银质针导热治疗后，MWT及TWL较模型中显著延长(P < 0.01)。与正常组相比，模型组自发电活动显著增加。银质针导热组自发电活动强度较模型组明显下降。与正常组相比，模型组海马齿状回神经元密度下降、排列紊乱并出现损伤，银质针导热治疗后上述形态学明显改善。与正常组相比，模型组海马突触超微结构受损，而银质针导热治疗可改善海马突触超微结构(P < 0.01)。与正常组相比，模型组海马 Syn 和 PSD-95 表达降低，而银质针导热治疗可上调其表达(P < 0.01)。结论：银质针导热疗法可提高 MPS 大鼠痛阈，减轻海马齿状回神经元损伤并改善海马突触超微结构及 Syn、PSD-95 表达；推测该疗法可能通过改善海马神经可塑性参与缓解 MPS 相关疼痛。

Abstract:

Objective: To investigate the effects of silver-needle conduction therapy on hippocampal neurons and synaptic plasticity in rats with myofascial pain syndrome, and to explore the potential central mechanisms by which it alleviates chronic pain. Methods: Twenty male Sprague–Dawley (SD) rats were randomly assigned, using a random number table, to a normal control group, a model group, and a silver-needle heat-conductive therapy group (n = 6 per group). The MPS model was established by blunt impact and eccentric exercise applied to the right vastus medialis muscle. Mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were assessed at 1 day before modeling (T0), and at weeks 4 (T1) and 8 (T2) after modeling, as well as 2 weeks after treatment (T3). Electromyographic activity of the right vastus medialis was recorded. Hematoxylin–eosin (H&E) and Nissl staining were used to evaluate neuronal morphology in the hippocampal dentate gyrus. Synaptic ultrastructure in the hippocampus was examined by transmission electron microscopy. PSD-95 and Syn protein expression was quantified by Western blotting. Results :Compared with the normal control group, the model group showed significantly decreased MWT and TWL (P < 0.01). After silver-needle heat-conductive therapy, MWT and TWL were significantly prolonged versus the model group (P < 0.05). Compared with the normal control group, spontaneous electrical activity was significantly increased in the model group, whereas its intensity was markedly reduced in the treatment group. In the hippocampal dentate gyrus, the model group exhibited reduced neuronal density, disorganized arrangement, and evident neuronal injury; these morphological changes were clearly ameliorated after treatment. Compared with the normal control group, hippocampal synaptic ultrastructure was impaired in the model group, and silver-needle heat-conductive therapy significantly improved synaptic ultrastructure (P < 0.01). Syn and PSD-95 expression in the hippocampus was reduced in the model group but was upregulated after treatment (P < 0.01). Conclusion :Silver-needle conductive heat therapy increased pain thresholds in MPS rats, attenuated neuronal injury in the hippocampal dentate gyrus, and improved hippocampal synaptic ultrastructure as well as the expression of synaptophysin (Syn) and postsynaptic density protein-95 (PSD-95). These findings suggest that this therapy may alleviate MPS-related pain, at least in part, by enhancing hippocampal neuroplasticity.