Photobiomodulation reduces neuropathic pain after spinal cord injury by downregulating CXCL10 expression

被引:13
作者
Zhang, Zhihao [1 ]
Zhu, Zhijie [1 ]
Zuo, Xiaoshuang [1 ]
Wang, Xuankang [1 ]
Ju, Cheng [1 ]
Liang, Zhuowen [1 ]
Li, Kun [1 ]
Zhang, Jiawei [1 ]
Luo, Liang [1 ]
Ma, Yangguang [1 ]
Song, Zhiwen [1 ]
Li, Xin [1 ,2 ]
Li, Penghui [1 ]
Quan, Huilin [1 ]
Huang, Peipei [1 ]
Yao, Zhou [1 ]
Yang, Ning [1 ]
Zhou, Jie [1 ]
Kou, Zhenzhen [3 ]
Chen, Beiyu [1 ]
Ding, Tan [1 ]
Wang, Zhe [1 ]
Hu, Xueyu [1 ]
机构
[1] Air Force Mil Med Univ, Xijing Hosp, Dept Orthoped, Xian 710032, Shaanxi, Peoples R China
[2] 967 Hosp Peoples Liberat Army Joint Logist Support, Dalian, Liaoning, Peoples R China
[3] Air Force Mil Med Univ, Sch Basic Med, Dept Anat Histol & Embryol, Xian, Shaanxi, Peoples R China
基金
中国国家自然科学基金;
关键词
CXCL10; glia cells; neuropathic pain; photobiomodulation; spinal cord injury; CENTRAL-NERVOUS-SYSTEM; CYTOCHROME-C-OXIDASE; RAT MODEL; ASTROCYTES; MICROGLIA; NEUROINFLAMMATION; NEUTRALIZATION; BRAIN; ACCUMULATION; CONTRIBUTES;
D O I
10.1111/cns.14325
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
BackgroundMany studies have recently highlighted the role of photobiomodulation (PBM) in neuropathic pain (NP) relief after spinal cord injury (SCI), suggesting that it may be an effective way to relieve NP after SCI. However, the underlying mechanisms remain unclear. This study aimed to determine the potential mechanisms of PBM in NP relief after SCI. MethodsWe performed systematic observations and investigated the mechanism of PBM intervention in NP in rats after SCI. Using transcriptome sequencing, we screened CXCL10 as a possible target molecule for PBM intervention and validated the results in rat tissues using reverse transcription-polymerase chain reaction and western blotting. Using immunofluorescence co-labeling, astrocytes and microglia were identified as the cells responsible for CXCL10 expression. The involvement of the NF-& kappa;B pathway in CXCL10 expression was verified using inhibitor pyrrolidine dithiocarbamate (PDTC) and agonist phorbol-12-myristate-13-acetate (PMA), which were further validated by an in vivo injection experiment. ResultsHere, we demonstrated that PBM therapy led to an improvement in NP relative behaviors post-SCI, inhibited the activation of microglia and astrocytes, and decreased the expression level of CXCL10 in glial cells, which was accompanied by mediation of the NF-& kappa;B signaling pathway. Photobiomodulation inhibit the activation of the NF-& kappa;B pathway and reduce downstream CXCL10 expression. The NF-& kappa;B pathway inhibitor PDTC had the same effect as PBM on improving pain in animals with SCI, and the NF-& kappa;B pathway promoter PMA could reverse the beneficial effect of PBM. ConclusionsOur results provide new insights into the mechanisms by which PBM alleviates NP after SCI. We demonstrated that PBM significantly inhibited the activation of microglia and astrocytes and decreased the expression level of CXCL10. These effects appear to be related to the NF-& kappa;B signaling pathway. Taken together, our study provides evidence that PBM could be a potentially effective therapy for NP after SCI, CXCL10 and NF-kB signaling pathways might be critical factors in pain relief mediated by PBM after SCI.
引用
收藏
页码:3995 / 4017
页数:23
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