糖尿病大鼠局灶性脑缺血再灌注对NF-κBp65表达的影响

Expression of NF-κBp65 after Focal Cerebral Ischemia Reperfusion in Diabetic Rats

目的:探讨阻断泛素蛋白酶体途径(ubiquitin proteasome pathway,UPP)对糖尿病大鼠局灶性脑缺血再灌注损伤的神经保护作用。方法:将Sprague-Dawley大鼠随机分成正常对照组(A组)、假手术组(B组)、非糖尿病组(C组)、糖尿病组(D组)、糖尿病治疗组(E组)及糖尿病治疗对照组(F组),链脲佐菌素腹腔注射制作糖尿病模型,线栓法制作大鼠大脑中动脉缺血2h再灌注模型;用clasto-lactacystin β-lactone阻断UPP,免疫组织化学方法观察再灌注24h后NF-κBp65的表达。结果:脑缺血再灌注24h后,NF-κBp65表达在D组较C组增加,在E组较D组和F组减少(P<0.05)。结论:糖尿病局灶性脑缺血NF-κBp65表达增多,阻断UPP可通过抑制NF-κBp65的活化而产生神经保护作用。

Objective：To study the mechanism of blocking ubiquition proteasome pathway （UPP） in protection of brain from ischemia reperfusion caused injury in diabetic rats. Methods：Sprague-Dawley （SD） rats were randomly divided into control group （group A）,sham operation group （group B）,non-diabetes cerebral infarction group （group C）,diabetes cerebral infarction group （group D）,diabetes cerebral infarction treatment group （group E） and diabetes cerebral infarction treatment control group （group F）. Diabetic model was made by injection of streptozotocin through abdomen. Transient focal cerebral ischemia reperfusion was produced by middle cerebral artery occlusion for 2 hours in SD rats. The UPP was blocked by clasto-lactacystin β-lactone. The expression of NF-κBp65 was detected by immunohistochemistry method in 24 h after reperfusion. Results：In 24 h after the reperfusion,expression of NF-κBp65 in group D was higher than in group C,and was lower in group E than in groups D and F （P0.05）. Conclusion：Expression of NF-κBp65 increases in diabetic cerebral ischemia reperfusion rats,and the blocking UPP may perform neuroprotection effect by inhibiting the activation of NF-κBp65.