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首页> 外文期刊>Molecular medicine reports >Amelioration of lung ischemia-reperfusion injury by JNK and p38 small interfering RNAs in rat pulmonary microvascular endothelial cells in an ischemia-reperfusion injury lung transplantation model
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Amelioration of lung ischemia-reperfusion injury by JNK and p38 small interfering RNAs in rat pulmonary microvascular endothelial cells in an ischemia-reperfusion injury lung transplantation model

机译：在缺血再灌注损伤肺移植模型中，JNK和P38小干扰RNA在大鼠肺部微血管内皮细胞中改善肺缺血再灌注损伤

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The inhibition of mitogen-activated protein kinases (MAPKs), including c-Jun NH2-terminal protein kinase (JNK), p38 MAPK (p38) and extracellular signal-regulated protein kinase 1/2 (ERK1/2), have an important effect on lung ischemia-reperfusion injury (IRI) during lung transplantation (LT). However, the way in which combined MAPK inhibition exerts optimal protective effects on lung IRI remains to be elucidated. Therefore, the present study evaluated the therapeutic efficacy of the inhibition of MAPKs in rat pulmonary microvascular endothelial cells (PMVECs) in an IRI model of LT. The rat PMVECs were transfected with small interfering RNAs (siRNAs) against JNK, p38 or ERK1/2. Cotransfection was performed with siRNAs against JNK and p38 in the J+p group, JNK and ERK1/2 in the J+E group, p38 and ERK1/2 in the p+E group, or all three in the J+p+E group. Non-targeting (NT) siRNA was used as a control. The PMVECs were then treated to induce IRI, and the levels of inflammation, apoptosis and oxidative stress were detected. Differences between compared groups were determined using Tukey's honest significant difference test. In all groups, silencing of the MAPKs was shown to attenuate inflammation, apoptosis and oxidative stress to differing extents, compared with the NT group. The J+p and J+p+E groups showed lower levels of interleukin (IL)-1, IL-6 and malondialdehyde, a lower percentage of early-apoptotic cells, and higher superoxide dismutase (SOD) activity, compared with the other groups. No significant differences were observed in the inflammatory response, SOD activity or early apoptosis between the J+p and J+p+E groups. These findings suggested that the dual inhibition of JNK and p38 led to maximal amelioration of lung IRI in the PMVECs of the IRI model of LT, which occurred through anti-inflammatory, anti-oxidative and anti-apoptotic mechanisms.
机译：抑制丝裂原活化蛋白激酶（MAPK），包括C-JUN NH2-末端蛋白激酶（JNK），P38MAPK（P38）和细胞外信号调节蛋白激酶1/2（ERK1 / 2）具有重要作用肺移植（LT）期间肺缺血再灌注损伤（IRI）。然而，组合的MAPK抑制对肺IRI产生最佳保护作用的方式仍有待阐明。因此，本研究评估了LT中的IRI模型中大鼠肺部微血管内皮细胞（PMVEC）抑制MAPK的治疗效果。用针对JNK，P38或ERK1 / 2的小干扰RNA（siRNA）转染大鼠PMVEC。在j + e组，P38和ERK1 / 2中，在j + e组，P38和ERK1 / 2中，在J + P组，JNK和ERK1 / 2中，在J + E组中的所有三个中，在J + e组，P38和ERK1 / 2中进行分致反应。或者在J + P + E中的所有三个团体。非靶向（NT）siRNA作为对照。然后处理PMVEC以诱导IRI，检测炎症，细胞凋亡和氧化胁迫的水平。使用Tukey诚实的显着差异测试确定比较组之间的差异。在所有组中，与NT组相比，显示MAPKS的沉默以衰减对不同植物的炎症，细胞凋亡和氧化应激。 J + P和J + P + E基团显示出较低水平的白细胞介素（IL）-1，IL-6和丙二醛，与另一个相比的更高凋亡细胞的较高百分比和更高的超氧化物歧化酶（SOD）活性。团体。在J + P和J + P + E组之间的炎症反应，SOD活性或早期凋亡中没有观察到显着差异。这些发现表明，JNK和P38的双重抑制导致LUNG IRI在LT的IRI模型的PMVEC中的最大化改善，这通过抗炎，抗氧化和抗凋亡机制发生。

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