Hydrogen-rich Saline Alleviated the Hyperpathia and Microglia Activation via Autophagy Mediated Inflammasome Inactivation in Neuropathic Pain Rats

•Neuropathic pain stimulated activation of inflammasome NLRP3 and autophagy pathway.•Hydrogen promoted autophagy activity and inhibited the inflammasome NLRP3 pathway activation.•Hydrogen treatment could alleviate hyperpathia by autophagy-mediated NLRP3 inactivation. 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.