comPhillygenin reduced neuropathic pain by inhibiting the rats’ TLR4/MyD88/NF-κB pathway.

To elucidate the effects of phillygenin (PHI) and the potential mechanism on TLR4 and MyD88/NF-κB signalling in neuropathic pain in an-imal studies, chronic constriction injury (CCI) models were constructed for neuropathic pain induction using male Sprague-Dawley rats. PHI (20 mg/kg) was delivered through intragastric administration. Von Frey and Hargreaves tests were implemented to determine the 50% paw-withdrawal threshold (PWT) and paw-withdrawal latency (PWL). A nitric oxide (NO) assay was used for NO level detection, and an ELISA assay was employed to measure the expression of proinflammatory cytokines. Western blotting and RT-qPCR were conducted for protein and mRNA level detection. Treatment with PHI significantly enhanced 50% of PWT and PWL. PHI significantly decreased the levels of NO and reduced the levels of TNF-α, IL -1β, and IL -6. PHI also downregulated TLR4 and MyD88 expressions and inhibited the phosphorylation of NF-κB.PHI ameliorated in-flammatory status and alleviated neuropathic pain in CCI rats, targeting TLR4 and suppressing MyD88/NF-κB signalling.