Objective To evaluate the role of spinal Toll-like receptor 4 (TLR4) signaling pathway in the development of inflammatory pain in rats.Methods Thirty-six adult male Sprague-Dawley rats were divided into 3 groups (n=12 each) using a random number table:control group,inflammatory pain group and TLR4 signaling pathway inhibitor epigallocatechin gallate (EGCG) group (EGCG group).Inflammatory pain was induced by injecting 50 μl of complete Freund's adjuvant (CFA) into the ankle joint cavity of the left hindpaw of rats anesthetized with isoflurane.At 1-3 days after injection of CFA,EGCG 30 μg was intrathecally injected once a day in group EGCG.At 1,3 (30 min after intrathecal injection),5and 7 days after injection of CFA,the mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured.The ipsilateral L4.5 segments of the spinal cord were removed at 3 days after CFA injcction for determination of TLR4 expression (by Western blot) and contents of tumor necrosis factor-alpha (TNF-oα),interleukin-6 (IL-6) and IL-1β in the spinal dorsal horn (by enzymelinked immunosorbent assay).Results Compared with control group,the MWT was significantly decreased and the TWL was shortened at each time point after injection of CFA,the expression of TLR4 in the spinal dorsal horn was up-regulated,and contents of TNF-α,IL-6 and IL-1β in the spinal dorsal horn were increased in inflammatory pain group (P＜ 0.05),and no significant change was found in the parameters mentioned above in EGCG group (P＞0.05).Compared with inflammatory pain group,the MWT was significantly increased and the TWL was prolonged at each time point after injection of CFA,the expression of TLR4 in the spinal dorsal horn was down-regulated,and contents of TNF-α,IL-6 and IL-1β in the spinal dorsal horn were decreased in EGCG group (P＜0.05).Conclusion Spinal TLR4 signaling pathway is involved in the development of inflammatory pain in rats.

Objective To investigate the analgesic effect of methane rich saline (MS) on monoarthritis (MA) rat and its possible mechanism.Methods We utilized Complete Freund's Adjuvant (CFA) to induce MApain model,and observed the effect of MS on MA rats by behavior assess,western blot,enzyme linked immunosorbent assay(ELISA),and oxidative stress assay.Results Intraperitoneal injections of MS attenuated MA-induced mechanical allodynia.MS treatments inhibited the activation of microglia and astrocytes,decreased IL-1β and TNF-α production in the spinal cord on day 10 post-operation.Additionally,MS also suppressed MA-induced oxidative stress (MDA),and protected the antioxidant capacity (SOD and CAT) in spinal cord dorsal horn.Conclusions Our findssuggested the analgesic effect of MS on monoarthritis pain,and imply antineuroinflammation and anti-oxidative stress as the associated mechanisms.

Objective To investigate the analgesic effect of methane rich saline (MS) on monoarthritis (MA) rat and its possible mechanism.Methods We utilized Complete Freund's Adjuvant (CFA) to induce MApain model,and observed the effect of MS on MA rats by behavior assess,western blot,enzyme linked immunosorbent assay(ELISA),and oxidative stress assay.Results Intraperitoneal injections of MS attenuated MA-induced mechanical allodynia.MS treatments inhibited the activation of microglia and astrocytes,decreased IL-1β and TNF-α production in the spinal cord on day 10 post-operation.Additionally,MS also suppressed MA-induced oxidative stress (MDA),and protected the antioxidant capacity (SOD and CAT) in spinal cord dorsal horn.Conclusions Our findssuggested the analgesic effect of MS on monoarthritis pain,and imply antineuroinflammation and anti-oxidative stress as the associated mechanisms.