小胶质细胞
自噬
神经病理性疼痛
炎症体
脊髓
化学
药理学
医学
炎症
麻醉
神经科学
免疫学
生物
生物化学
细胞凋亡
精神科
作者
Hongguang Chen,Chunjing Zhou,Keliang Xie,Xiaoyin Meng,Yaoqi Wang,Yonghao Yu
出处
期刊:Neuroscience
[Elsevier BV]
日期:2019-11-01
卷期号:421: 17-30
被引量:51
标识
DOI:10.1016/j.neuroscience.2019.10.046
摘要
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.
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