Department of Anesthesiology, Tianjin Medical University General Hospital, Tianjin 300052, China; Tianjin Research Institute of Anesthesiology, Tianjin 300052, China.
Department of Anesthesiology, Tianjin 4th Center Hospital, Tianjin 300140, China.
Neuroscience. 2019 Nov 21;421:17-30. doi: 10.1016/j.neuroscience.2019.10.046. Epub 2019 Nov 2.
Neuropathic pain is a complication after a spinal nerve injury. The inflammasomes are now identified to be responsible for triggering inflammation in neuropathic pain. Autophagy participates in the process of neuropathic pain and can regulate the inflammasome activation in different diseases. Our previous research reported that hydrogen exerted a protective effect against neuropathic pain. Therefore, we focused on the mechanism and role of autophagy and inflammasome, by which hydrogen alleviated the hyperpathia induced by neuropathic pain. The results showed that neuropathic pain stimulated activation of inflammasome NLRP3 and autophagy pathway in the microglial cells of the spinal cord. The inhibition of NLRP3 inhibited the hyperpathia induced by spinal nerve litigation surgery. The absence of autophagy aggravated the inflammasome activity and hyperpathia. Hydrogen promoted autophagy related protein expression, inhibited the inflammasome NLRP3 pathway activation, and relieved the hyperpathia induced by neuropathic pain. Hydrogen treatment could alleviate hyperpathia by autophagy-mediated NLRP3 inactivation.
神经病理性疼痛是脊髓神经损伤后的一种并发症。现在已经确定炎性小体负责引发神经病理性疼痛中的炎症。自噬参与神经病理性疼痛的过程，并能在不同疾病中调节炎性小体的激活。我们之前的研究报告表明，氢气对神经病理性疼痛具有保护作用。因此，我们专注于自噬和炎性小体的机制和作用，研究氢气如何缓解神经病理性疼痛引起的痛觉过敏。结果表明，神经病理性疼痛刺激脊髓小胶质细胞中炎性小体 NLRP3 和自噬途径的激活。NLRP3 的抑制抑制了由脊神经损伤手术引起的痛觉过敏。自噬的缺失加重了炎性小体的活性和痛觉过敏。氢气促进了自噬相关蛋白的表达，抑制了炎性小体 NLRP3 途径的激活，缓解了神经病理性疼痛引起的痛觉过敏。氢气治疗可以通过自噬介导的 NLRP3 失活来缓解痛觉过敏。
