發(fā)布時(shí)間：2018-04-03 10:36

  本文選題：腦缺血再灌注　切入點(diǎn)：c-Jun氨基末端激酶(JNK)　出處：《中國老年學(xué)雜志》2017年18期

【摘要】：目的探討c-Jun氨基末端激酶(JNK)在大鼠腦缺血再灌注(CIR)損傷中的作用。方法構(gòu)建CIR大鼠模型,同時(shí)在大鼠腦側(cè)室給予JNK抑制劑-SP600125抑制JNK的激活。采用5分制對造模后的大鼠行為學(xué)評分,用2,3,5-氯化三苯基四氮唑(TTC)染色分析大鼠CIR后腦梗死體積。原位末端標(biāo)記(TUNEL)法檢測大鼠腦組織中神經(jīng)細(xì)胞凋亡情況,Western印跡檢測大鼠腦組織中B細(xì)胞淋巴瘤(Bcl)-2、Bax、裂解的天冬氨酸特異性半胱氨酸蛋白酶(酶切-caspase)3、白細(xì)胞介素(IL)-1β、腫瘤壞死因子(TNF)-α、JNK蛋白表達(dá)水平。結(jié)果模型組CIR損傷后3、24、72 h行為學(xué)評分均明顯高于假手術(shù)組(P0.01),說明成功構(gòu)建了大鼠CIR模型。實(shí)驗(yàn)組CIR損傷后3、24、72 h行為學(xué)評分均明顯低于模型組(P0.01)。腦梗死再灌注后3、24和72 h模型組大鼠腦組織中腦梗死體積、細(xì)胞凋亡率均明顯高于假手術(shù)組,實(shí)驗(yàn)組均明顯低于模型組(均P0.01)。模型組腦組織中Bax、酶切-caspase3蛋白表達(dá)水平均明顯高于假手術(shù)組,Bcl-2蛋白表達(dá)水平明顯低于假手術(shù)組(P0.01)。實(shí)驗(yàn)組中Bax、酶切-caspase3蛋白表達(dá)水平均明顯低于模型組,Bcl-2蛋白表達(dá)水平明顯高于模型組(均P0.01)。實(shí)驗(yàn)組JNK的表達(dá)水平低于模型組(P0.01)。模型組大鼠腦組織中IL-1β、TNF-α水平均明顯高于假手術(shù)組,實(shí)驗(yàn)組均明顯低于模型組(均P0.01)。結(jié)論抑制JNK激活可以減輕大鼠CIR損傷,作用機(jī)制可能與Bcl-2、Bax、酶切-caspase3表達(dá)有關(guān)。
[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- 偽 -JNK protein in TNF- 偽.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- 偽 in the brain tissue of the model group was significantly higher than that of the sham operation group, and the level of TNF- 偽 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.
【作者單位】： 石河子大學(xué)醫(yī)學(xué)院第一附屬醫(yī)院老干二科;
【基金】：新疆維吾爾自治區(qū)自然科學(xué)基金項(xiàng)目(2012213A063)
【分類號】：R743.3

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