异丙酚对大鼠局灶性脑缺血/再灌注损伤期炎性细胞因子的影响

Effect of propofol on tumor necrosis factor-alpha,interleukin-6,interleukin-8 in rats following cerebral ischemia-reperfusion

目的 :探讨脑缺血再灌注损伤中肿瘤坏死因子 -α(TNF -α)、白细胞介素 - 6 (IL - 6 )、白细胞介素 - 8(IL - 8)含量的变化及异丙酚 (propofol)对它们的影响。 方法 :72只成年Wistar大鼠随机分为 3组 ,A组为假手术组 (n =8) ;B组为对照组(n =32 ) ,在缺血前 10min腹腔注射生理盐水 10ml/kg ,脑缺血 2h后 ,分为 4小组 (n =8) ,分别再灌注 1h、6h、12h、2 4h ;C组为异丙酚组 ,在缺血前 10min腹腔注射异丙酚 10 0mg/kg ,脑缺血 2h后 ,分组同B组。观察血浆中TNF -α、IL - 6、IL - 8、丙二醛(MDA) ,超氧化物歧化酶 (SOD)含量的变化 ,取大脑组织HE染色 ,光镜观察。结果 :异丙酚组的TNF -α、IL - 6、IL - 8、MDA含量明显低于对照组 (P <0 .0 5 ) ,而SOD活性高于对照组。光镜下异丙酚组的细胞结构尚完整 ;对照组细胞损伤严重。结论 :异丙酚抑制脑缺血再灌注时炎性细胞因子的表达 ,从而减轻细胞因子介导的炎性损伤 。

Objective:To explore changes of tumor necrosis factor alpha (TNF-α),interleukin-6 (IL-6),interleukin-8 (IL-8) in plasma and the effect of propofol on these cytokines in rats following cerebral ischemia-reperfusion injury.Methods:Focal cerebral ischemia model was induced by occluding the middle cerebral artery (MCA).Seventy two adult Wistar rats were divided randomly into three groups:sham operation group (group A),control group ( group B),which was intraperitoneally infused with 0.9% saline (10ml·kg -1 ) before ischemia and subdiuided into four groups two hours after ischemia and reperfused respectively for one hour,six hours,twelve hours,and twenty-four hours.Propofol group (group C),which was intraperitoneally infused with propofol (100mg.kg -1 ) before ischemia and reperfusion.The serum concentration of TNF-α,IL-6,IL-8 and malondialdehyde (MDA) contents and activities of superoxide dismutase (SOD) were measured.Hematoxylin and eosin staining for the cerebral tissue was processed.Results:The serum concentration of TNF-α,IL-6,IL-8 and MDA of propofol group were significantly lower than control group,while the activity of SOD in plasma was higher than control group.Under light microscope,the structure of cells remained perfect in propofol group,while the cells of control group showed swelling,karyorrhexis and karyolysis.Conclusion:In addition to antioxidation,propofol effectively suppresses the production and release of inflammatory cytokine,and therefore protect the brain from ischemia and reperfusion injury.