Objective      To determine the effects of quercetin (Que) on neuropathic pain in rats after chronic constriction injury (CCI)

and investigate its underlying mechanisms. Methods      A total of 80 SD rats were randomly divided into control (n=8)

sham operation (n=18)

and CCI model group (n=56). In 7 d after model establishment

Que was given intragastrically at 30

50 and 100 mg/kg. Before and in 3

7

14

21 and 28 d after treatment

the mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were determined by behavioral test in neuropathic pain rat models of CCI. Spinal production of TNF-α and IL-1β was quantified by ELISA kits. The protein and mRNA expression levels of iNOS

COX-2

Wnt3a and β-catenin were determined by qRT-PCR and Western blotting

respectively. Results      Compared with control and sham operation group

the MWT and TWL were decreased significantly in the CCI group (P0.05)

while the spinal contents of TNF-α and IL-1β

the expression levels of the pain associated molecules iNOS and COX-2

and WNT pathway molecules

Wnt3a and βcatenin were all up-regulated (P0.05). However

Que treatment also markedly increased the MWT and TWL

inhibited the production of TNF-α and IL-1β

and suppressed the expression of iNOS

COX-2

Wnt3a and β-catenin (P0.05)

in a dose-dependent manner. Whereas

the activator of Wnt/β-catenin pathway could block the effect of Que to the CCI rats. Conclusion      Que may alleviate neuropathic pain in CCI rats by inhibiting Wnt/β-catenin signal pathway and downstream molecules COX-2 and iNOS.