基于转录组学的电针治疗肌筋膜疼痛综合征模型大鼠的作用机制研究  

Mechanism of Transcriptomics-based Electroacupuncture in the Treatment of Myofascial Pain Syndrome in Rats

作　　者：王列[1,2] 李记泉 马帅[3] 于嘉祥 马俊杰[1,2] 胡哲 李格格 陈怡然 王鹰 卞镝[1,2] 马铁明 董宝强[1,2] 于本性 王树东[1,2] WANG Lie;LI Jiquan;MA Shuai;YU Jiaxiang;MA Junjie;HU Zhe;LI Gege;CHEN Yiran;WANG Ying;BIAN Di;MA Tieming;DONG Baoqiang;YU Benxing;WANG Shudong(Liaoning University of Traditional Chinese Medicine,Shenyang 110847,China;Key Laboratory of Acupuncture Moxibustion and Health Rehabilitation in Liaoning Province,Shenyang 110847,China;Shenyang Seventh People′s Hospital,Shenyang 110847,China)

机构地区：[1]辽宁中医药大学,沈阳110847 [2]辽宁省针灸养生康复重点实验室,沈阳110847 [3]沈阳市第七人民医院,沈阳110847

出　　处：《世界中医药》2024年第24期3775-3784,共10页World Chinese Medicine

基　　金：国家自然科学基金项目(82205253);辽宁省科技厅博士启动课题(2023-BS-137)。

摘　　要：目的:探索电针治疗肌筋膜疼痛综合征(MPS)的疗效和作用机制。方法:分别设置空白组、模型组、电针组,采用钝性打击结合离心运动方式复制MPS大鼠模型,对电针组进行电针干预。取材前进行各组大鼠自发电活动频率、热缩足潜伏期检测;取材后通过酶联免疫吸附试验(ELISA)法检测各组大鼠血清中超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)水平;苏木精-伊红(HE)染色法观察各组大鼠肌肉组织病理形态;以各组大鼠的脊髓组织为研究对象进行转录组学测序;应用平行反应监视技术(PRM)对序列相似家族111成员A(FAM111A)、含锌指和BTB结构域的蛋白16(ZBTB16)、蛋白磷酸酶1调节因子亚基3G(PPP1R3G)、围脂滴蛋白4(PLIN4)、蛋白磷酸酶1调节亚基3C(PPP1R3C)共5个蛋白进行定量。结果:电针干预能减轻MPS造成的病理损伤,恢复骨骼肌组织形态,升高大鼠血清SOD、GSH-Px、CAT水平,降低MDA、IL-1β、IL-6、TNF-α水平。MPS模型大鼠87个基因的mRNA表达水平发生变化,涉及到了钙离子等信号通路。电针干预能升高FAM111A的表达水平,降低ZBTB16、PPP1R3G、PLIN4、PPP1R3C的表达水平。结论:电针干预MPS有效,电针治疗MPS的具体机制可能与抑制炎症反应、氧化应激和调控能量代谢有关,修复因MPS造成的病理损伤。Objective:To explore the efficacy and mechanism of electroacupuncture(EA)in treating myofascial pain syndrome(MPS).Methods:A blank group,model group,and EA group were set up.The MPS rat model was established using blunt force and centrifugal exercise methods.The EA group received EA intervention.Spontaneous electrical activity frequency and hot-plate latency were measured before tissue collection.After treatment,enzyme-linked immunosorbent assay(ELISA)was used to detect serum levels of superoxide dismutase(SOD),malondialdehyde(MDA),glutathione peroxidase(GSH-Px),catalase(CAT),interleukin-1β(IL-1β),interleukin-6(IL-6),and tumor necrosis factor-α(TNF-α).Hematoxylin and eosin(HE)staining was used to observe muscle tissue histopathological morphology.Spinal cord tissues from the rats were subjected to transcriptomic sequencing.Parallel reaction monitoring(PRM)technology was applied to quantify the expression levels of five proteins:family with sequence similarity 111 member A(FAM111A),zinc finger and BTB domain-containing protein 16(ZBTB16),protein phosphatase 1 regulatory subunit 3G(PPP1R3G),perilipin 4(PLIN4),and protein phosphatase 1 regulatory subunit 3C(PPP1R3C).Results:EA intervention alleviated pathological damage caused by MPS,restored skeletal muscle tissue morphology,and increased serum levels of SOD,GSH-Px,and CAT,while reducing MDA,IL-1β,IL-6,and TNF-αlevels.The mRNA expression levels of 87 genes in the MPS model rats changed,involving calcium ion signaling pathways.EA intervention increased the expression of FAM111A and decreased the expression of ZBTB16,PPP1R3G,PLIN4,and PPP1R3C.Conclusion:EA is effective in treating MPS,and its therapeutic mechanism may involve inhibiting inflammatory response,oxidative stress,and regulating energy metabolism to repair pathological damage caused by MPS.

关 键 词：肌筋膜疼痛综合征 电针 治疗 脊髓组织 转录组学 平行反应监视技术 炎症反应 氧化应激 

分 类 号：R245[医药卫生—针灸推拿学] R274.3[医药卫生—中医临床基础]