Blocking NLRP3 inflammasome expression by RAS-like protein A mitigates neuropathic pain in chronic constriction injury rat models

Purpose: To investigate the role of RAS-like protein A (RalA) in lipopolysaccharide-induced inflammatory regulation primary microglia chronic constriction injury (CCI)-induced neuropathic pain rat models.
 Methods: In vitro, overexpression (OE) RalA was performed using transfection procedure, and then LPS used to provoke phenotype. vivo, model induced CCI treated with LV-RalA. Neuroinflammatory levels including expressions IL-1β, IL-6, TNF-α were detected. Moreover, NF-κB p65, thioredoxin-interacting (TXNIP) NLR family pyrin domain-containing 3(NLRP3)were examined rats microglial cells. Finally, functional evaluation determined via mechanical allodynia thermal hyperalgesia assays.
 Results: The level decreased dorsal horn following CCI. OE after insult CCI-induced significantly inflammation promoters (p < 0.05). Mechanistically, mitigated response by inhibiting NF-κB/TXNIP/NLRP3 signaling pathway, thus attenuating cells rats.
 Conclusion: These results indicate that plays a protective NF-κB/TXNIP/ NLRP3 axis. findings may provide promising therapeutic target for pain.