【摘要】 目的探讨黄芪提取物(EA)对大鼠全脑缺血再灌注损伤的保护机制。方法用四动脉阻断法,制备大鼠全脑缺血再灌注模型;采用Western blot检测大鼠全脑缺血再灌注6h后脑皮层组织NFκBp65和IκBα的表达;采用免疫组化(SP法)检测大鼠全脑缺血再灌注24h后脑皮层组织ICAM-1、TNF-α的表达。结果与假手术组相比,模型组大鼠全脑缺血再灌注后脑皮层组织核蛋白NFκBp65(107.1±24.18vs313.09±23.35,P<0.05)表达明显增多,而胞浆蛋白NFκBp65(221.72±19.44vs125.82±25.07,P<0.05)、IκBα(382.98±55.21vs184.37±20.40,P<0.05)表达明显减少;EA可升高大鼠全脑缺血再灌注后脑皮层组织胞浆蛋白NFκBp65、IκBα表达、降低核蛋白NFκBp65表达;同时可降低脑皮层组织ICAM-1、TNF-α的表达。结论EA的脑保护机制可能与抑制大鼠全脑缺血再灌注后NFκBp65活化及降低脑皮质中ICAM-1、TNF-α的表达有关。更多还原

【Abstract】 Objective To explore the mechanisms of neuro-protection effects of astragalus extract(EA) in global cerebral ischemia and reperfusion (I/R) rats.Methods Rats were pretreated ig EA for 5 d and then subjected to global cerebral I/R by four-vessel occlusion method.Expressions of NFκBp65, IκBα in cortex tissue of I/R rats were evaluated with Western blot, and the expressions of ICAM-1 and TNF-α of the cortex tissue were examined by immunohistochemical technical in I/R rats.Results EA increased the expressions of neucleoprotein NFκBp65 (107.1±24.18 vs 313.09±23.35,P<0.05) and decreased the expression of plasmosin NFκBp65 (221.72±19.44 vs 125.82±25.07,P<0.05),IκBα (382.98±55.21 vs 184.37±20.40,P<0.05).Compared with control group,ICAM-1 and TNF-α expressions during I/R of the group treated with EA were significantly decreased.Conclusion EA has protective effects on cerebral injury through inhibiting the activation of NFκB and decreasing the cortex expressions of ICAM-1 and TNF-α after I/R injury.更多还原