Department of Exercise Physiology, Faculty of Sport Sciences, Shahid Chamran University of Ahvaz, Ahvaz, Iran.
Graduate of Exercise Physiology, Shahid Chamran University of Ahvaz, Ahvaz, Iran.
Contrast Media Mol Imaging. 2022 May 18;2022:6551358. doi: 10.1155/2022/6551358. eCollection 2022.
Nervous inflammation is an important component of the pathogenesis of neurodegenerative diseases including chronic diabetic neuropathic pain. In order to obtain a decrease in the progression of diabetic neuronal damage, it may be necessary to examine therapeutic options that involve antioxidants and anti-inflammatory agents. The aim of this study was to investigate the attenuation of inflammatory factors with endurance training in the spinal cord of rats with neuropathic pain. Thirty-two 8-week-old male Wistar rats (with a weight range of 204 ± 11.3 g) were randomly divided into 4 groups ( = 8), including (1) diabetic neuropathy (50 mg/kg streptozotocin intraperitoneal injection), (2) diabetic neuropathy training (30 minutes of endurance training at 15 meters per minute, 5 days a week for 6 weeks), (3) healthy training, and (4) healthy control. After confirmation of diabetic neuropathy by behavioral tests, training protocol and supplementation were performed. The NLRP3, P38 MAPK, TNF-, and IL-1 gene expressions were measured by a real-time technique in the spinal cord tissue. One-way analysis of variance and Tukey's post hoc test were used for statistical analysis. Endurance training reduced the sensitivity of the nervous system to thermal hyperalgesia and mechanical allodynia; also, compared to the diabetic neuropathy group, the gene expressions of NLTP3, P38 MAPK, TNF-, and IL-1 were significantly reduced by endurance training ( < 0.05). Endurance training modulates NLRP3, P38 MAPK, and TNF-, IL-1 gene expressions and improves the sensitivity of nociceptors to pain factors. Accordingly, it is recommended to use endurance training to reduce neuropathic pain for diabetics.
神经炎症是包括慢性糖尿病神经性疼痛在内的神经退行性疾病发病机制的重要组成部分。为了减缓糖尿病神经元损伤的进展，可能需要研究涉及抗氧化剂和抗炎剂的治疗选择。本研究旨在探讨耐力训练对神经病理性疼痛大鼠脊髓炎症因子的衰减作用。将 32 只 8 周龄雄性 Wistar 大鼠（体重范围为 204±11.3g）随机分为 4 组（每组 8 只），包括（1）糖尿病神经病变（50mg/kg 链脲佐菌素腹腔注射）、（2）糖尿病神经病变训练（15m/min 耐力训练 30 分钟，每周 5 天，持续 6 周）、（3）健康训练和（4）健康对照。通过行为测试确认糖尿病神经病变后，进行训练方案和补充。采用实时技术测量脊髓组织中 NLRP3、P38MAPK、TNF-α 和 IL-1 基因的表达。采用单因素方差分析和 Tukey 事后检验进行统计学分析。耐力训练降低了神经系统对热痛觉过敏和机械性痛觉过敏的敏感性；与糖尿病神经病变组相比，耐力训练还显著降低了 NLTP3、P38MAPK、TNF-α 和 IL-1 的基因表达（<0.05）。耐力训练调节 NLRP3、P38MAPK 和 TNF-α、IL-1 基因表达，提高伤害感受器对疼痛因子的敏感性。因此，建议使用耐力训练来减轻糖尿病患者的神经性疼痛。
