地塞米松对大鼠局灶性脑缺血再灌注损伤模型TNF-α表达的干预

Intervention of dexamethasone on TNF-αexpression of focal cerebral injury following ischemia and reperfusion in rats

目的研究地塞米松对大鼠局灶性脑缺血再灌注损伤模型肿瘤坏死因子(TNF-α)表达的影响。方法大脑中动脉线栓法复制局灶性脑缺血再灌注模型。实验随机分为3组:(1)正常假手术组。(2)生理盐水组。(3)地塞米松组犤0.5mg/(kg·d)犦。生理盐水组与地塞米松组分别于缺血2h后再灌6,12,24,48h。采用HE、免疫组化及酶联免疫吸附实验(ELISA)等方法观察地塞米松对缺血再灌性脑损伤脑组织TNF-α表达的影响。结果脑缺血再灌注性损伤后TNF-α阳性细胞数,生理盐水组和地塞米松组各时间点明显多于假手术组(3.0±7.2)(q=9.38～17.98,P<0.01),再灌注6,12h,地塞米松组(45.1±5.4,81.4±17.4)明显多于生理盐水组(34.2±7.2,60.4±15.4)(q=4.67,P<0.01;q=3.50,P<0.05)。结论脑缺血再灌注后TNF-α表达的增强可能是地塞米松加重缺血再灌注性脑损伤的机制之一。

Aim To investigate the effects of dexamethasone on TNF αexpression of focal cerebral injury following ischemia and reperfusion in rats.Methods Middle cerebral artery ischemia/reperfusion rat's models were induced by using modified filament method.Wistar rats were divided randomly:(1)Sham group;(2)Dexamethasone group [0.5 mg/(kg·d)];(3)Saline group,Dexamethasone and saline groups were reperfused for 6, 12 , 24, 48 hours after ischemia for 2 hours. HE staining, immunohistochemistry and ELISA were performed to observe the effects of dexamethasone on injury and TNF αprotein expression.Results The number of TNF αpositive cells in sham group was 3.0±1.2,and 34.2±7.2,60.4±15.4,47.6±9.3,55.6±12.4 in saline group,45.1±5.4,81.4±17.4,44.0±10.9,51.6±15.7 in dexamethason group at ischemia 2 h reperfusion 6,12,24,48 h,with significant difference among saline,dexamethason and sham group(q=9.38-17.98,P< 0.01),and there were an obviously significant difference between saline and dexamethason group at reperfusion 6 h(q=4.67,P< 0.01),and a significant difference at reperfusion 12 h(q=3.50,P< 0.05) respectively.Conclusion High expression of TNF αmay play an important role in dexamethasone aggravating ischemia/reperfusion injury.