选择性COX2抑制剂对脑缺血再灌注损伤的影响

Effects of Specific COX2 Inhibitor on Ischemic Brain Injury

目的 :观察脑缺血再灌注损伤中COX2的表达以及选择性COX2抑制剂SC5 812 5对脑缺血再灌注后脑梗死体积、PGE2 含量的影响。方法 :应用小鼠短暂性局灶性脑缺血模型 ;脑梗死体积的测定采用TTC染色法 ;ELISA测定PGE2 含量 ;DNA单链损伤的测定采用PANT染色。结果 :缺血前 3 0min和缺血后 2h用药组脑梗死体积显著缩小 ,缺血后 6h延迟用药组脑梗死体积无明显变化。脑缺血再灌注后PGE2 含量显著升高。SC5 812 5的治疗显著降低了PGE2 的水平。SC5 812 5并可显著抑制缺血后DNA单链损伤的程度。结论 :提示COX2参与了脑缺血再灌注损伤 。

Aim:The role of prostaglandin synthesis enzyme COX2 in mediating ischemic brain injury was investigated. Methods:The model of focal ischemia/reperfusion was used in the mouse. The infarction volumes were evaluated by TTC staining. The content of PGE 2 and the extent of DNA damage were measured by ELISA and PANT method respectively. Results:Administration of selective COX2 inhibitor, SC58125, prior to or 2 h after but not 6 h after MCA occlusion significantly reduced the levels of PGE 2 content and the infarct volume as measurement at 72 h after ischemia. Tissue contents of PGE 2 were significantly increased in the brain of ischemic territory following MCA occlusion and reperfusion, indicating that COX2 activity was induced in the ischemic brain. DNA single strand breaks, a marker of oxidative cellular injury, was also significantly decreased in animals treated with SC58125.Conclusion:COX2 mediates ischemic/reperfusion injury, the selective COX2 inhibitor SC58125 has an important role in treatment of focal ischemia/reperfusion in mouse.