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首页> 外文期刊>Life sciences >Transduction of anti-cell death protein FNK protects isolated rat hearts from myocardial infarction induced by ischemia/reperfusion
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Transduction of anti-cell death protein FNK protects isolated rat hearts from myocardial infarction induced by ischemia/reperfusion

机译：抗细胞死亡蛋白FNK的转导可保护离体大鼠心脏免受缺血/再灌注所致的心肌梗塞

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摘要

Artificial anti-cell death protein FNK, a Bcl-xL derivative with three amino acid-substitutions (Y22F, Q26N, and R165K) has enhanced anti-apoptotic and anti-necrotic activity and facilitates cell survival in many species and cell types. The objectives of this study were (i) to investigate whether the protein conjugated with a protein transduction domain (PTD-FNK) reduces myocardial infarct size and improves post-ischemic cardiac function in ischemic/reperfused rat hearts, and (ii) to understand the mechanism(s) by which PTD-FNK exerts a protective effect. Isolated rat hearts were subjected to 35-min global ischemia, followed by 120-min reperfusion using the Langendorff methods. PTD-FNK (a total of 30 μl) was injected intramuscularly into the anterior wall of the left ventricle either at 1 min after induction of global ischemia (group A) or at 30 min after induction of global ischemia (at 5 min before reperfusion) (group B). In group A, infarct size was significantly reduced from 47.8 ± 6.8% in the control to 30.4 ± 5.2, 28.7 ± 3.8, and 30.4 ± 6.8% with PTD-FNK at 5, 50, and 500 nmol/l, respectively (p < 0.05). Temporal recovery of left ventricular developed pressure at 60 min and 120 min after reperfusion was significantly better in PTD-FNK (50 and 500 nmol/l)-treated groups than in the control (p < 0.05). In contrast, PTD-FNK treatment had no effect on group B. Western blot analysis showed that PTD-FNK markedly inhibited procaspase-3 cleavage (activation of caspase-3) and reduced the number of nuclei stained by a terminal deoxynucleotidyl transferase-mediated deoxyuridine 5-triphoshate nick-end labeling (TUNEL) assay. These findings suggest that PTD-FNK reduces the volume of myocardial infarction with corresponding functional recovery, at least in part, through the suppression of myocardial apoptosis following ischemia/reperfusion.
机译：人工抗细胞死亡蛋白FNK是具有三个氨基酸取代基（Y22F，Q26N和R165K）的Bcl-xL衍生物，具有增强的抗凋亡和抗坏死活性，并有助于许多物种和细胞类型的细胞存活。这项研究的目的是（i）研究与蛋白转导结构域（PTD-FNK）偶联的蛋白是否能减少缺血/再灌注大鼠心脏的心肌梗塞面积并改善缺血后的心脏功能，以及（ii）了解PTD-FNK发挥保护作用的机制。离体的大鼠心脏经受了35分钟的整体缺血，然后使用Langendorff方法进行了120分钟的再灌注。在诱导全脑缺血后1分钟（A组）或诱导全脑缺血后30分钟（再灌注前5分钟）将PTD-FNK（总共30μl）肌肉注射到左心室前壁（B组）。在A组中，使用5、50和500 nmol / l的PTD-FNK时，梗塞面积从对照组的47.8±6.8％显着降低至30.4±5.2、28.7±3.8和30.4±6.8％（p < 0.05）。 PTD-FNK（50和500 nmol / l）治疗组在再灌注后60分钟和120分钟时左心室发育压力的时间恢复明显好于对照组（p <0.05）。相反，PTD-FNK处理对B组没有影响。蛋白质印迹分析表明PTD-FNK显着抑制procaspase-3裂解（激活caspase-3）并减少了末端脱氧核苷酸转移酶介导的脱氧尿苷染色的核数。 5-三磷酸酯缺口末端标记法（TUNEL）。这些发现表明，PTD-FNK至少部分地通过抑制缺血/再灌注后的心肌细胞凋亡来减少心肌梗塞的体积并具有相应的功能恢复。

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