Huang Yuanxin, Huang Yuanyue, Lv Xianglong, Yu Zilong, Qin Yue, Yang Xingyue, An Songsong, Wo Chunxin, Wang Lin
Pain Department, Affiliated Hospital of Guizhou Medical University, No. 28, Guiyi Street, Liu Guang Men, Guiyang, 550004, Guizhou, China.
Clinical Medicine School, Guizhou Medical University, Guiyang, 550004, Guizhou, China.
Eur J Med Res. 2024 Dec 5;29(1):578. doi: 10.1186/s40001-024-02134-6.
Patients with neuropathic pain (NP) have significantly lower quality of life. Because the pathophysiology of NP is not fully understood, there is a lack of effective treatment for it in clinic. This study set out to investigate the precise mechanism by which pulsed radiofrequency (PRF) alleviated NP.
The rat models of chronic constriction injury of the sciatic nerve (CCI) were established to simulate the occurrence of NP, following with measuring MWT and TWL to evaluate the pain of the rats. HE staining was utilized to observe the rat spinal cord tissue pathology. The expression of MG53, ATF4 and CHOP was evaluated by qRT-PCR and WB, while the expression of inflammatory factors was measured by ELISA. In addition, immunofluorescence assay was used to detect the expression of MG53 and Iba-1.
PRF treatment alleviated NP in CCI rats, as well as upregulating the expression of MG53 and inhibiting microglial activation. After MG53 knockdown, the remission of NP by PRF was significantly weakened, but microglial activation and endoplasmic reticulum stress (ERS) exhibited enhancement. Therefore, PRF inhibited microglial activation by upregulating MG53. After injection of ERS inducer in CCI rats, the inhibition effect of overexpressed MG53 on microglial activation and its alleviation effect on NP were reversed. Consequently, MG53 played a role in suppressing microglial activation by mediating the inhibition of ERS.
PRF attenuated microglial activation by upregulating MG53 to inhibit ERS, resulting in the alleviation of NP in CCI rats.
神经性疼痛（NP）患者的生活质量显著较低。由于NP的病理生理学尚未完全明确，临床上缺乏有效的治疗方法。本研究旨在探究脉冲射频（PRF）缓解NP的精确机制。
建立坐骨神经慢性压迫损伤（CCI）大鼠模型以模拟NP的发生，随后测量机械缩足阈值（MWT）和热缩足潜伏期（TWL）以评估大鼠疼痛程度。采用苏木精-伊红（HE）染色观察大鼠脊髓组织病理学变化。通过实时定量聚合酶链反应（qRT-PCR）和蛋白质免疫印迹法（WB）评估MG53、活化转录因子4（ATF4）和C/EBP同源蛋白（CHOP）的表达，同时采用酶联免疫吸附测定法（ELISA）检测炎症因子表达。此外，利用免疫荧光法检测MG53和离子钙接头蛋白1（Iba-1）的表达。
PRF治疗可缓解CCI大鼠的NP，同时上调MG53表达并抑制小胶质细胞活化。MG53基因敲低后，PRF对NP的缓解作用显著减弱，但小胶质细胞活化和内质网应激（ERS）增强。因此，PRF通过上调MG53抑制小胶质细胞活化。在CCI大鼠中注射ERS诱导剂后，过表达MG53对小胶质细胞活化的抑制作用及其对NP的缓解作用被逆转。因此，MG53通过介导ERS的抑制在抑制小胶质细胞活化中发挥作用。
PRF通过上调MG53抑制ERS从而减弱小胶质细胞活化，进而缓解CCI大鼠的NP。
