Huang Y, An S, Tang Y, Yang X, Shen C, Huang Y, Wang L, Wo C
Guizhou Medical University, Guiyang, China, Pain Department, The Affiliated Hospital of Guizhou Medical University, Guiyang, China.
Physiol Res. 2025 Jul 23;74(3):481-492.
The objective of this study is to elucidate the therapeutic mechanisms underlying silver needle thermal therapy (SNT) in alleviating skeletal muscle mitochondrial damage in a rat model of myofascial pain syndrome (MPS), with particular emphasis on its regulatory role concerning TRPV1/CaMKII. The MPS rat model was established through blunt impact and eccentric movement. Interventions included SNT and local intramuscular injections of anti-TRPV1 miRNA. Behavioral assessments were conducted to measure the mechanical and thermal pain thresholds of the rats. Histopathological staining was performed to evaluate muscle structure, while mitochondrial damage was assessed using transmission electron microscopy. Western blotting analysis was employed to quantify expression levels of TRPV1, CaMKII, and CytC. Additionally, immunofluorescence techniques were applied to analyze both the expression levels of TRPV1 and its co-localization with CaMKII. Following administration of SNT and anti-TRPV1 miRNA injections, a downregulation in the expression levels of TRPV1, CaMKII, and CytC within the muscle tissue of MPS rats was observed; concurrently, mitochondrial damage exhibited improvement. The implementation of SNT and the inhibition of TRPV1 lead to a reduction in CaMKII, thereby alleviating mitochondrial damage, indicating that TRPV1 is a potential target for silver needle thermal therapy of MPS. Key words SNT " MPS " Mitochondria " TRPV1 " CaMKII.
本研究的目的是阐明银质针导热疗法(SNT)在缓解肌筋膜疼痛综合征(MPS)大鼠模型骨骼肌线粒体损伤中的治疗机制,特别强调其对瞬时受体电位香草酸亚型1(TRPV1)/钙调蛋白依赖性蛋白激酶II(CaMKII)的调节作用。通过钝性撞击和离心运动建立MPS大鼠模型。干预措施包括SNT和局部肌肉注射抗TRPV1微小核糖核酸(miRNA)。进行行为评估以测量大鼠的机械性和热痛阈值。进行组织病理学染色以评估肌肉结构,同时使用透射电子显微镜评估线粒体损伤。采用蛋白质免疫印迹分析来量化TRPV1、CaMKII和细胞色素C(CytC)的表达水平。此外,应用免疫荧光技术分析TRPV1的表达水平及其与CaMKII的共定位。给予SNT和抗TRPV1 miRNA注射后,观察到MPS大鼠肌肉组织中TRPV1、CaMKII和CytC的表达水平下调;同时,线粒体损伤有所改善。实施SNT和抑制TRPV1导致CaMKII减少,从而减轻线粒体损伤,表明TRPV1是MPS银质针导热疗法的潜在靶点。关键词:SNT;MPS;线粒体;TRPV1;CaMKII