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首页> 外文期刊>Life sciences >Involvement of mitogen-activated protein kinases (MAPKs) during testicular ischemia-reperfusion injury in nuclear factor-kappa B knock-out mice
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Involvement of mitogen-activated protein kinases (MAPKs) during testicular ischemia-reperfusion injury in nuclear factor-kappa B knock-out mice

机译：核因子-κB基因敲除小鼠睾丸缺血再灌注损伤过程中丝裂原活化蛋白激酶（MAPKs）的参与

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Nuclear factor kappa-B (NF-kappa B), extracellular regulated kinase (ERK 1/2) and c-jun-N terminal kinase (JNK) play an important role in testicular ischemia. We investigated the patterns of ERK 1/2, JNK and p38 activation in NF-KB knockout (KO) mice subjected to testicular torsion. KO and normal littermate wild-type (WT) animals underwent at I h testicular ischemia followed by 24 h reperfusion (TI/R). Sham testicular ischemia-reperfusion mice served as controls. ERK 1/2, INK and p38 expression by western blot analysis, tumor necrosis factor-alpha (TNF-alpha) expression (RT-PCR and western blot analysis) and a complete histological examination were carried out. TI/R caused a greater increase in phosphorylated form of ERK 1/2 in KO mice than in WT animals in either the ischemic testis and the contralateral one. By contrary, active form of JNK and p38 were completely abrogated in both testes of KO mice, while WT animals showed a significant activation of those kinases in both testes. TNF-alpha expression was markedly reduced in KO mice when compared to WT mice either at the mRNA and the protein level. Finally TI/R-induced histological damage was markedly reduced in KO mice. Our data indicate that NF-KB plays a pivotal role in the development of testicular ischemia-reperfusion injury and suggest that, in the absence of the transcriptional factor, the up-stream signal JNK and p38 may be abrogated while ERK 1/2 activity is enhanced. (c) 2007 Elsevier Inc. All rights reserved.
机译：核因子κB（NF-κB），细胞外调节激酶（ERK 1/2）和c-jun-N末端激酶（JNK）在睾丸缺血中起重要作用。我们调查了睾丸扭转的NF-KB基因敲除（KO）小鼠中ERK 1/2，JNK和p38激活的模式。 KO和正常同窝野生型（WT）动物在1 h睾丸局部缺血后再进行24 h再灌注（TI / R）。假睾丸缺血再灌注小鼠作为对照。通过Western印迹分析，肿瘤坏死因子-α（TNF-alpha）表达（RT-PCR和Western印迹分析）和完整的组织学检查，进行ERK 1/2，INK和p38表达。在缺血性睾丸和对侧睾丸中，TI / R在KO小鼠中引起的ERK 1/2磷酸化形式的增加比在WT动物中增加。相反，在KO小鼠的两个睾丸中，JNK和p38的活性形式被完全消除，而WT动物在两个睾丸中均显示出这些激酶的显着激活。与WT小鼠相比，无论是在mRNA还是在蛋白水平上，KO小鼠中的TNF-α表达均显着降低。最后，在KO小鼠中，TI / R诱导的组织学损伤明显减少。我们的数据表明，NF-KB在睾丸缺血再灌注损伤的发展中起着关键作用，并表明，在缺乏转录因子的情况下，上游信号JNK和p38可能被废除，而ERK 1/2活性却被消除。增强。 （c）2007 Elsevier Inc.保留所有权利。

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