Objective To observe the effect of intrathecal p38 MAPK inhibitor(SB203580) treatment on neuropathic pain and the expression of p38 MAPK and BDNF in dorsal horn of spinal cord in rats with chronic constriction injury(CCI),So as to investigate the possible mechanisms of neuropathic pain.Methods Totally 30 SD rats were evenly randomized into 3 groups(n=10) :sham group receiving intrathecal injection of sodium chloride,control group receiving intrathecal injection of sodium chloride and CCI surgery,and SB203580 group receiving intrathecal injection of SB203580 and CCI surgery.SB203580(0.1 ml/kg) was administered 0.5 h before and 1-14 d after CCI surgery.The mechanical thresholds were tested 24 h before and 4-14 d after CCI surgery.p38 MAPK expression and BDNF release in the dorsal horn were determined using immunohistochemistry method 14 d after CCI surgery.Results The mechanical thresholds in the control and SB203580 groups were significantly lower after CCI surgery compared with that before CCI surgery(P0.05).Compared with the sham operation group,the mechanical thresholds were significantly lower in the other two groups after CCI surgery(P

Objective To investigate the effect of propofol pretreatment on hypoxia-induced apoptosis of alveolar epithelial type Ⅱ (AE Ⅱ) cells in fetal rats. Methods Primary cultured AE Ⅱ cells isolated from fetal rats were seeded in 96-well plates (1 × 106/L, 180 μl/well) and randomly assigned to one of 3 groups (n = 72each):normal control group (group C), hypoxia group (group H) and propofol-hypoxia group (group P-H).Group H and P-H were exposed to hypoxia (5% O2). In group P-H, propofol (final concentration 5 μ mol/L) was added 1 h prior to hypoxia (5% O2). The apoptotic rate and expression of hypoxia-inducible factor (HIF)-1αmRNA, Bnip3L mRNA, HIF-1α protein and Bnip3L protein were determined at 3, 12, 24 and 48 h of hypoxia.Results The apoptotic rate and expression of HIF-1α mRNA, Bnip3L mRNA, HIF-lα protein and Bnip3L protein were significantly up-regulated in group H compared with group C (P ＜ 0.05). Propofol pretreatment could significantly inhibit the hypoxia-induced changes mentioned above (P ＜ 0.05). Conclusion Propofol pretreatment can inhibit hypoxia-induced apoptosis of AE Ⅱ cells, and the mechanism is related to inhibition of HIF-1αactivation and down-regulation of Bnip3L expression in fetal rats.