c-Jun氨基末端激酶在大鼠脑缺血再灌注损伤中的作用及机制

发布时间：2018-04-03 10:36

本文选题：脑缺血再灌注　切入点：c-Jun氨基末端激酶(JNK)　出处：《中国老年学杂志》2017年18期

【摘要】：目的探讨c-Jun氨基末端激酶(JNK)在大鼠脑缺血再灌注(CIR)损伤中的作用。方法构建CIR大鼠模型,同时在大鼠脑侧室给予JNK抑制剂-SP600125抑制JNK的激活。采用5分制对造模后的大鼠行为学评分,用2,3,5-氯化三苯基四氮唑(TTC)染色分析大鼠CIR后脑梗死体积。原位末端标记(TUNEL)法检测大鼠脑组织中神经细胞凋亡情况,Western印迹检测大鼠脑组织中B细胞淋巴瘤(Bcl)-2、Bax、裂解的天冬氨酸特异性半胱氨酸蛋白酶(酶切-caspase)3、白细胞介素(IL)-1β、肿瘤坏死因子(TNF)-α、JNK蛋白表达水平。结果模型组CIR损伤后3、24、72 h行为学评分均明显高于假手术组(P0.01),说明成功构建了大鼠CIR模型。实验组CIR损伤后3、24、72 h行为学评分均明显低于模型组(P0.01)。脑梗死再灌注后3、24和72 h模型组大鼠脑组织中脑梗死体积、细胞凋亡率均明显高于假手术组,实验组均明显低于模型组(均P0.01)。模型组脑组织中Bax、酶切-caspase3蛋白表达水平均明显高于假手术组,Bcl-2蛋白表达水平明显低于假手术组(P0.01)。实验组中Bax、酶切-caspase3蛋白表达水平均明显低于模型组,Bcl-2蛋白表达水平明显高于模型组(均P0.01)。实验组JNK的表达水平低于模型组(P0.01)。模型组大鼠脑组织中IL-1β、TNF-α水平均明显高于假手术组,实验组均明显低于模型组(均P0.01)。结论抑制JNK激活可以减轻大鼠CIR损伤,作用机制可能与Bcl-2、Bax、酶切-caspase3表达有关。
[Abstract]:Objective to investigate the role of c-Jun aminoterminal kinase (c-Jun) in cerebral ischemia-reperfusion injury in rats.Methods the rat model of CIR was established and the activation of JNK was inhibited by JNK inhibitor-SP600125 at the same time.The behavioral score of the model rats was evaluated by 5 points system, and the infarct volume of rats after CIR was analyzed by TTC staining.In situ terminal deoxynucleotidyl transferase Nick end labeling (Tunel) assay for the detection of neuronal apoptosis in rat brain tissue and Western blotting for detection of B cell lymphoma in rat brain tissue Bcl-2P Bax.The cleavage of aspartate specific cysteine proteinase (caspase-3), interleukin-1 尾 (IL-1- 尾), and swelling were detected by Western blot.Expression of TNF- 伪 -JNK protein in TNF- 伪.Results the behavioral scores in the model group were significantly higher than those in the sham operation group at 72 h after CIR injury, indicating that the rat model of CIR was successfully constructed.The behavioral scores in the experimental group were significantly lower than those in the model group at 72 h after CIR injury (P 0.01).The cerebral infarction volume and apoptosis rate in the model group were significantly higher than those in the sham-operation group at 3h and 72h after reperfusion (P < 0.01), and those in the experimental group were significantly lower than those in the model group (P < 0.01).The expression of Bax-caspase-3 protein in brain tissue of model group was significantly higher than that of sham-operated group (P 0.01).The expression of Bax-caspase-3 protein in the experimental group was significantly lower than that in the model group (P 0.01).The expression of JNK in the experimental group was lower than that in the model group (P 0.01).The level of IL-1 尾 -TNF- 伪 in the brain tissue of the model group was significantly higher than that of the sham operation group, and the level of TNF- 伪 in the experimental group was significantly lower than that in the model group (all P 0.01).Conclusion inhibiting the activation of JNK can attenuate the damage of CIR in rats, and the mechanism may be related to the expression of Bcl-2Caspase-3.
【作者单位】：石河子大学医学院第一附属医院老干二科;
【基金】：新疆维吾尔自治区自然科学基金项目(2012213A063)
【分类号】：R743.3

【相似文献】