摘要
目的:探讨JNK3信号通路在亚低温治疗脑缺血再灌注性损伤中的作用及其具体机制。方法:采用四动脉阻断法诱导大鼠全脑缺血,将SD大鼠随机分为假手术组、缺血再灌注对照组、亚低温处理组、SP600125(JNK3抑制剂)处理组及溶剂组;采用亚甲基蓝染色检测大鼠缺血再灌注后海马CA1区神经元的损伤情况;采用免疫印迹法检测脑组织中JNK3及c-jun蛋白的磷酸化水平。结果:亚低温处理组、SP600125(JNK3抑制剂)处理组与缺血再灌注对照组相比海马CA1区神经元损伤明显减轻,蛋白JNK3、c-jun磷酸化水平显著降低(P<0.05)。结论:亚低温治疗通过抑制脑缺血再灌注损伤后JNK3的磷酸化激活参与了对海马CA1区神经元的保护性作用。
AIM： To investigate the role of JNK3 on neuroprotective effect of Hypothermia in the CA1 region of the adult rat after ischemia-reperfusion. METHODS： Models with cerebral ischemiareperfusion were induced using four-vessel occlusion and received 10 min ischemia. Rats were randomly divided into several groups,including sham-operation,ischemia-reperfusion,Hypothermia pretreated ischemia-reperfusion,SP600125 pretreated ischemia-reperfusion and Vehicle pretreated ischemia-reperfusion. Histological assessment of neuronal damage in the CA1 field was performed via Staining with Toluidine blue. Western blotting was operated to detect expression of JNK3 and c-jun. RESULTS： In the CA1 field,both groups of Hypothermia pretreated and SP600125 pretreated,not only ischemiareperfusion injury was alleviated,but also expressions of p-JNK3 and p-c-jun were down-regulated,compared to ischemia-reperfusion only group. CONCLUSION： Hypothermia inhibits post-ischemic cell death in region of CA1 by down-regulated phosphorylation of JNK3 and its downstream effectors.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2015年第6期611-615,共5页
Chinese Journal of Clinical Pharmacology and Therapeutics
