摘要
目的:研究地塞米松是否加重脑缺血再灌注细胞凋亡及核转录因子NF-κB、Caspase-3在此过程中的作用。方法:采用线栓法建立大鼠局灶性脑缺血再灌注模型。缺血1h后生理盐水组腹腔注射0.9%氯化钠注射液(0.5mL),地塞米松组腹腔注射地塞米松[0.5mg(/kg·d)]。利用TUNEL法研究凋亡细胞的变化,应用免疫组化、原位杂交法检测NF-κB蛋白、Caspase-3mRNA的表达。结果:各缺血组凋亡细胞显著增多。地塞米松组各时点凋亡细胞数多于生理盐水组,NF-κB活化程度均明显低于生理盐水组,Caspase-3染色阳性细胞数明显高于生理盐水组(P<0.01)。结论:地塞米松加重大鼠局灶性脑缺血再灌注损伤可能是与其阻碍NF-κB蛋白活化与上调Caspase-3mRNA表达,并继而加重脑神经细胞凋亡的机制有关。
Objective: To investigate the effects of dexamethasone on the expressions of NF-κB and Caspase-3 in cell apop-tosis of focal cerebral ischemia and repeffusion injury. Methods: The rat models of focal cerebral ischemia and repeffusion were established by middle cerebral artery occlusion. Experimental group was treated with dexamethasone [0.5 mg/ (kg·d)] and the control group was treated with saline (0.5 mL) one hour after ischemia. Cell apoptosis was studied by TUNEL and the expressions of NF-κB and Caspase-3 were examined by immunohistochemistry and hybridization. Results: The number of apoptotic cell increased significantly in ischemia groups. The expression of NF-κB protein decreased significantly, Caspase-3 positive cells increased significantly and the number of TUNEL-positive apoptotic cells increased significantly in dexamethasone group compared with those in saline group (P 〈 0.01 ). Conclusion: Down-regulating the expression of NF-κB protein and up-regulating the expression of Caspase-3 mRNA may be the causes of dexamethasone aggravating focal cerebral ischemia and repeffusion injury.
出处
《天津医药》
CAS
北大核心
2007年第9期681-683,共3页
Tianjin Medical Journal