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目的:通过观察细胞因子TNF-α、IL-1β、IL-1Ra指标,研究丹参酮对脊髓缺血再灌注损伤免疫途径的干预作用。方法:将新西兰家兔12只,随机分为单纯缺血再灌注组(模型组)、丹参酮干预组(丹参酮组)。采用Zivin法改进复制模型,于造模前1h治疗;丹参酮组,腹腔注射丹参酮。模型组,不做治疗处理。各组家兔分别于治疗前、缺血30min再灌注后0.5h、1h、4h、8h、12h分别采家兔股静脉血。检测:血清TNF-α、IL-1β、IL-1Ra指标。结果:模型组,家兔血清TNF-α、IL-1β、IL-1Ra各时点均升高,与正常时比较差异有统计学意义(P<0.05)。丹参酮组与模型组比较TNF-α、IL-1β降低(P<0.05);IL-1Ra升高(P<0.05)。结论:家兔脊髓缺血再灌注损伤后,可导致家兔血清TNF-α、IL-1β、IL-1Ra升高。丹参酮对脊髓缺血再灌注损伤免疫途径的干预作用是通过降低TNF-α、IL-1β,升高IL-1Ra,从而对脊髓神经功能有一定的保护作用。丹参酮治疗存在时间窗效应。
OBJECTIVE: To investigate the effects of tanshinones on the immunological pathways of spinal cord ischemia-reperfusion injury by observing the cytokines TNF-α, IL-1β and IL-1Ra. Methods: Twelve New Zealand rabbits were randomly divided into simple ischemia-reperfusion group (model group) and tanshinone intervention group (tanshinone group). The Zivin method was used to improve the replication model and was treated at 1 hour before modeling. Tanshinone group was injected intraperitoneally with tanshinone. Model group, not treated. Rabbits in each group were respectively given femoral vein blood samples before treatment, 0.5h, 1h, 4h, 8h, 12h after ischemia 30 min reperfusion. Detection: serum TNF-α, IL-1β, IL-1Ra indicators. Results: The levels of TNF-α, IL-1β and IL-1Ra in model group and rabbit at each time point were significantly higher than those in normal group (P <0.05). Compared with model group, tanshinone group decreased TNF-α and IL-1β (P <0.05) and increased IL-1Ra (P <0.05). Conclusion: Rabbits spinal cord ischemia-reperfusion injury, can lead to rabbit serum TNF-α, IL-1β, IL-1Ra increased. Tanshinone can decrease the level of TNF-α, IL-1β and increase the level of IL-1Ra in the spinal cord after ischemia-reperfusion injury, which can protect neurons from spinal cord injury. Tanshinone treatment has time window effect.