按压对慢性激痛点模型大鼠线粒体自噬水平及PINK1/Parkin通路的影响

关键词：按压  激痛点  骨骼肌  线粒体  线粒体自噬  能量代谢

Keywords:pressing  myofascial trigger point  skeletal muscle  mitochondria  mitochondrial autophagy  energy metabolism

摘要：

      摘要 目的：通过观察按压对慢性激痛点模型大鼠骨骼肌线粒体自噬水平的影响，探讨按压对激痛点去活化的作用机制。 方法：30只SPF级大鼠随机分为空白组（n=10）和激痛点模型组(n=20)，以钝性打击配合离心运动法复制激痛点模型，造模成功后符合评价标准者将其随机分为模型组（n=10）和按压组（n=10），按压组以自制按法刺激器干预14d，干预结束后取其激痛点骨骼肌组织，以试剂盒测定线粒体膜电位（mitochondrial membrane potential， MMP）、柠檬酸合酶（citrate synthase， CS）、线粒体复合物I和三磷酸腺苷（adenosine triphosphate， ATP）含量，以免疫印迹法检测微管相关蛋白1轻链3-I（microtubule-associated protein 1 light chain 3-I， LC3-I）、LC3-II、泛肽结合蛋白1(sequestosome protein1， P62)、UNC51-类似自噬激活激酶1 (UNC-51 like autophagy activating kinase 1， ULK1)、p-ULK1、磷酸酶及张力蛋白同源物诱导的蛋白激酶1(PTEN induced putative kinase 1， PINK1)与Parkin蛋白表达。 结果：与空白组相比，模型组MMP、CS、线粒体复合物I、ATP水平均下降（P＜0.05），LC3-II、LC3-II/LC3-I比值与P62表达上升（P＜0.05）；与模型组相比，按法组MMP、CS、线粒体复合物I、ATP、LC3-II、LC3-II/LC3-I比值、p-ULK、p-ULK1/ULK1、PINK1与Parkin水平均上升（P＜0.05），P62表达下降（P＜0.05）。 结论：按压激痛点可以恢复局部线粒体功能，改善局部能量代谢，达到激痛点去活化效应，其机制可能与PINK1/Parkin通路提高线粒体自噬有关。

Abstract:

      Abstract Objective： To observe the effect of pressing on skeletal muscle mitochondrial autophagy of chronic pain point in rat， and to explore the mechanism of deactivation of myofascial trigger point (MTrP) by pressing. Method： Thirty SPF rats were randomly divided into blank group (n=10) and MTrP model group (n=20). The MTrP model was reproduced by blunt struck combined with centrifugal exercise. Those who met the evaluation criteria were randomly divided into model group (n=10) and pressing group (n=10). The pressing group was intervened with self-made pressing stimulator for 14 days， and the skeletal muscle tissue of MTrP was taken after the intervention. The mitochondrial membrane potential (MMP)， citrate synthase (CS)， mitochondrial complex I and adenosine triphosphate (ATP) content were detected by kit. Western blotting was used to detect the expression of microtubule-associated protein 1 light chain 3-I (LC3-I)， LC3-II， sequestosome protein1 (P62)， UNC-51 like autophagy activating kinase 1 (ULK1)， p-ULK1， PTEN induced putative kinase 1 (PINK1) and parkin protein. Result： Compared with the blank group， the levels of MMP， CS， mitochondrial complex I and ATP in the model group decreased (P＜0.05) and the LC3-II， LC3-II/ LC3-I and expression of p62 increased (P＜0.05). Compared with the model group， the levels of MMP， CS， mitochondrial complex I， ATP， LC3II， LC3-II/ LC3-I， p-ULK， p-ULK1/ULK1， PINK1 and Parkin increased (P＜0.05) while the expression of p62 decreased(P＜0.05) in the pressing group. Conclusion： Pressing the MTrP can restore the local mitochondrial function， improve the local energy metabolism to achieve the deactivation effect， which may be related to the activation of mitochondrial autophagy by PINK1/Parkin pathway.