| Literature DB >> 31689487 |
Hongguang Chen1, Chunjing Zhou2, Keliang Xie1, Xiaoyin Meng3, Yaoqi Wang1, Yonghao Yu4.
Abstract
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.Entities:
Keywords: autophagy; hydrogen; inflammasome; neuropathic pain
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Year: 2019 PMID: 31689487 DOI: 10.1016/j.neuroscience.2019.10.046
Source DB: PubMed Journal: Neuroscience ISSN: 0306-4522 Impact factor: 3.590