Abstract:Objective To observe the effects of dehydrocorinine (DHC) on hyperalgesia and spinal cord inflammatory cytokine expression in chronic inflammatory pain mice. Methods According to the random number table method, 30 male ICR mice were divided into three groups: Sham group, complete Freund’s adjuvant (CFA) group and CFA+DHC group, with ten mice in each group. Mice in Sham group were subcutaneously injected with 25 μL normal saline in the middle of the right hind paw. Mice in CFA group and CFA+DHC group were subcutaneously injected with 25 μL CFA into the middle part of right hind paw. From one to seven days after modeling, mice in the CFA+DHC group were intraperitoneally injected with 10 mg/kg DHC every day, and mice in the CFA group were intraperitoneally injected with solvent, and the paw withdrawal mechanical threshold (PWMT) and paw withdrawal latency (PWL) of the mice were determined 30 min after drug administration. On the seventh day, lumbar enlargement was taken, and the protein expressions of the proinflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6 and anti-inflammatory cytokines IL-10 were detected by Western blot. Results Overall analysis showed that there were statistically significant differences in the inter-group comparison, time point comparison and interaction between PWMT and PWL (all P < 0.05). Further comparisons were made in pairs. Intra-group comparison: comparison of PWMT and PWL before and after modeling in Sham group showed no statistically significant difference (P > 0.05). After modeling, the PWMT of CFA group and CFA+DHC group were lower than those before modeling, and the PWL was shorter than those before modeling, with statistically significant differences (all P < 0.05). Comparison between groups: before modeling, the basic values of PWMT and PWL of the three groups showed no statistically significant difference (P > 0.05). From one to seven days after modeling, compared with CFA group, PWMT and PWL in CFA+DHC group were increased and prolonged, and the differences were statistically significant (all P < 0.05). Compared with the CFA group, the expression levels of proinflammatory cytokines TNF-α, IL-1β and IL-6 in the CFA+DHC group were decreased, while the expression levels of anti-inflammatory cytokines IL-10 were increased, with statistically significant differences (P < 0.05). Conclusion DHC can effectively relieve hyperalgesia of chronic inflammatory pain induced by CFA in mice, and the mechanism may be related to inhibition of the expression of proinflammatory cytokines TNF-α, IL-1β, and IL-6 and increase of the expression of anti-inflammatory cytokines IL-10.