Objective To evaluate the effects of hydrogen-rich saline on chronic inflammatory pain in rats.Methods Thirty-two male Sprague-Dawley rats,aged 8-10 weeks,weighing 200-250 g,were randomly divided into 4 groups (n =8 each) using a random number table:control group (group C);complete Freund's adjuvant (CFA) group;hydrogen-rich saline group (group H2);CFA + hydrogenrich saline group (CFA+H2 group).Chronic inflammatory pain was induced by injecting CFA 100 μl into the plantar surface of the left hindpaw in CFA and CFA + H2 groups.In H2 and CFA + H2 groups,0.6 mmol/L hydrogen-rich saline 5 ml/kg was injected intraperitoneally once a day for 7 consecutive days starting from 1 day after injection of CFA,while the equal volume of normal salinc was given instead of hydrogen-rich saline in C and CFA groups.The mechanical paw withdrawal threshold (MWT) and thermal paw withdrawal latency (TWL) were measured at 1 day before CFA injection and 1,3 and 7 days after CFA injection.The rats were sacrificed after the last measurement of pain threshold on day 7 after CFA injection.The left lumbar segments (L4 5) of the spinal cord were removed for determination of nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) expression by Western blot.Results Compared with C group,no significant change was found in the MWT,TWL and expression of Nrf2 and HO-1 in H2 group,and the MWT was significantly decreased,the TWL was shortened,and the expression of Nrf2 and HO-1 was up-regulated in CFA and CFA+H2 groups.Compared with CFA group,the MWT was significantly increased,the TWL was prolonged,and the expression of Nrf2 and HO-1 was up-regulated in CFA+H2 group.Conclusion Hydrogen-rich saline can alleviate chronic inflammatory pain in rats,and activation of Nrf2/ARE signaling pathway in the spinal cord is involved in the mechanism.

Objective To evaluate the role of extracellular signal-related kinase (ERK) 1/2 signal transduction pathway at the supraspinal level in maintenance of neuropathic pain in mice.Methods Sixty-four Kunming mice,aged 2 months,weighing 18-20 g,were randomly divided into 4 groups (n =16 each):sham operation group (group S),chronic constrictive injury (CCI) group; CCI + U0126 (MEK inhibitor) group; CCI + dimethyl sulfoxide (DMSO) group.Neuropathic pain was induced by CCI.The sciatic nerve was exposed and 4 loose ligatures were placed on the sciatic nerve at 1mmintervals with 4-0 silk thread in CCI,CCI + U0126 and CCI +DMSO groups.On 5 days after CCI,5 μg U0126 (in 5 μl of 5％ DMSO) and 5％ DMSO 5 μl were injected into the lateral cerebral ventricle over 10 s in CCI + U0126 and CCI + DMSO groups,respectively,and the time of.needle retaining was 20 s.Paw withdrawal threshold to mechanical stimulation with yon Frey filament (MWT) and paw withdrawal latency to thermal stimulation (TWL) were measured before operation (baseline),before intracerebroventricular injection (T1),and at 30 min and 2,6,12 and 24h after intracerebroventricular injection (T2-6).Resuits Compared with group S,MWT was significantly decreased and TWL was shortened at T1-6 in CCI and CCI +DMSO groups,and at T1 in CCI + U0126 group (P ＜ 0.05),while no significant change in MWT and TWL was found at T2-6 in group CCI + U0126 (P ＞ 0.05).Compared with group CCI,MWT was significantly increased and TWL was prolonged at T2-6 in group CCI + U0126 (P ＜ 0.05),while no significant change in MWT and TWL was found in group CCI + DMSO (P ＞ 0.05).Conclusion ERK1/2 signaling transduction pathway at the supraspinal level is involved in maintenance of neuropathic pain in mice.