Exercise intervention alleviates nerve injury by the suppression of inflammatory mediator expression via the TLR4/NF-κB signaling pathway

被引:13
作者
Sun, Yan [1 ,2 ]
Liu, Jie Qiong [3 ]
Tian, Feng [1 ,2 ]
机构
[1] Sichuan Acad Med Sci, Emergency Dept, 32 West Second Sect First Ring, Chengdu 610072, Sichuan, Peoples R China
[2] Sichuan Prov Peoples Hosp, 32 West Second Sect First Ring, Chengdu 610072, Sichuan, Peoples R China
[3] Shandong Prov Peoples Hosp, Dept Pediat, Zoucheng 610041, Shandong, Peoples R China
关键词
spinal cord injury; glial fibrillary acidic protein; nuclear factor-kappa B; exercise; SPINAL-CORD-INJURY; NEUROTROPHIC FACTOR EXPRESSION; FUNCTIONAL RECOVERY; NOGO-A; HYPERTENSIVE-RATS; BLOOD-CELLS; KAPPA-B; TRANSPLANTATION; ELECTROACUPUNCTURE; NEUROPROTECTION;
D O I
10.3892/etm.2018.6581
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Spinal cord injury (SCI) may cause changes that have damaging effects on sensation and functionality. However, methods for the significant amelioration of SCI-reduced nerve injury are lacking. Previous studies have indicated that reasonable and effective exercise may promote the recovery of injured nerves. Therefore, the aim of the present study was to investigate the ability of exercise to improve recovery following SCI and the underlying mechanism. A rat model was used to evaluate the effects of two different periods of exercise intervention on recovery following SCI. The exercise intervention comprised 15 or 30 min/day passive walking for 30 days. ELISA measurements were used to analysis the plasma levels of inflammatory cytokines. Reverse transcription-quantitative polymerase chain reaction and western blot analyses were performed to examine the levels of proteins and mRNAs associated with nuclear factor (NF)-B-related signaling. In addition, histological examination and immunostaining were used to evaluate the neural injury and associated indicators. The results indicated that severe SCI induced a peripheral inflammatory response and increased the expression of inflammatory cytokines. In addition, the SCI-induced nerve injury was associated with increased glial fibrillary acidic protein (GFAP) expression and the upregulation of Toll-like receptor 4 (TLR4)/NF-B signaling, which may further aggravate the inflammatory responses induced by SCI. However, the exercise intervention decreased SCI-induced GFAP expression and reduced the activation of the TLR4/NF-B signaling pathway compared with that of SCI model rats that did not exercise. Furthermore, the exercise intervention inhibited the release of inflammatory cytokines into the serum. These results indicate that exercise treatment reduces inflammation and glial activation, and may be beneficial to recovery following SCI.
引用
收藏
页码:2922 / 2930
页数:9
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