褪黑素对急性脊髓损伤大鼠脊髓组织丙二醛以及血清炎性因子水平的影响

Effects of melatonin on spinal malondialdehyde and serum inflammatory cytokines levels in rats with acute spinal cord injury

目的观察褪黑素对急性脊髓损伤大鼠脊髓组织丙二醛以及血清白细胞介素(IL)-6、IL-8水平的影响。方法选取成年雄性SD大鼠108只,随机分为空白对照组、模型组、治疗组各36只。空白对照组大鼠仅切除T11椎板,不损伤脊髓,模型组与治疗组大鼠采用改良Allen氏重物坠落法建立T11脊髓损伤模型。模型组与治疗组大鼠于脊髓损伤后10 min分别腹腔注射无水乙醇和100 mg/kg褪黑素,空白对照组给予等体积生理盐水。于给药后1 h、6 h、12 h、24 h、48 h检测大鼠血清IL-6及IL-8、脊髓组织丙二醛水平,取大鼠脊髓组织观察病理变化。结果与空白对照组比较,模型组与治疗组大鼠脊髓组织均明显充血,但治疗组细胞水肿程度较模型组轻。在术后各个时间点,模型组、治疗组、空白对照组脊髓组织丙二醛、血清IL-6及IL-8的水平依次降低(均P <0. 05)。结论褪黑素可以减轻急性脊髓损伤大鼠的炎症反应与氧化应激反应。

Objective To observe the effects of melatonin on the spinal malondialdehyde and serum interleukin(IL)-6 and IL-8 in the rats with acute spinal cord injury.Methods A total of 108 adult male SD rats were randomly divided into blank control group,model group and treatment group,with 36 rats in each group.Resection of vertebral laminae T 11 was performed without spinal cord injury in the blank control group,while the modified Allen′s weight drop method was used to set up the rat model of T11 spinal cord injury in the model group and treatment group.The rats in the model group and treatment group were intraperitoneally injected with absolute ethanol and 100 mg/kg melatonin,respectively,at 10 minutes after spinal cord injury,and the blank control group was given normal saline of the same volume.After 1,6,12,24 and 48 hours of administration,the levels of serum IL-6 and IL-8 and spinal malondialdehyde were tested,the pathological changes in spinal cord tissues of the rats were observed.Results Compared with the blank control group,significant hyperemia was observed in spinal cord tissues of the rats in the model group and treatment group,but the treatment group suffered milder cellular edema compared with the model group.The levels of spinal malondialdehyde,serum IL-6 and IL-8 decreased in turn in the model group,the treatment group and the blank control group at each time point after operation(all P<0.05).Conclusion Melatonin can reduce the inflammatory reaction and oxidative stress response in the rats with acute spinal cord injury.