Ischemia–reperfusion injury has been proven to induce organ dysfunction and death, although the mechanism is not fully understood. Long non-coding RNAs (lncRNAs) have drawn wide attention with their important roles in the gene expression of some biological processes and diseases, including myocardial ischemia–reperfusion (I/R) injury. In this paper, a total of 26 Sprague–Dawley (SD) rats were randomized into two groups: sham and ischemia–reperfusion (I/R) injury. Hemorrhagic shock was induced by removing 45% of the estimated total blood volume followed by reinfusion of shed blood. High-throughput RNA sequencing was used to analyze differentially expressed (DE) lncRNAs and messenger RNAs (mRNAs) in the heart tissue 4 h after reperfusion. Myocardial function was also evaluated. After resuscitation, the decline of myocardial function of shocked animals, expressed by cardiac output, ejection fraction, and myocardial performance index (MPI), was significant (p < 0.05). DE lncRNAs and mRNAs were identified by absolute value of fold change ≥ 2 and the false discovery rate ≤ 0.001. In rats from the I/R injury group, 851 lncRNAs and 1015 mRNAs were significantly up-regulated while 1533 lncRNAs and 1702 m RNAs were significantly down-regulated when compared to the sham group. Among the DE lncRNAs, we found 12 location-associated with some known apoptosis-related protein-coding genes which were up-regulated or down-regulated accordingly, including STAT3 and Il1r1. Real time PCR assays confirmed that the expression levels of five location-associated lncRNAs (NONRATT006032.2, NONRATT006033.2, NONRATT006034.2, NONRATT006035.2 and NONRATT029969.2) and their location-associated mRNAs (STAT3 and Il1r1) in the rats from the I/R injury group were all significantly up-regulated versus the sham group. The DE lncRNAs (NONRATT006032.2, NONRATT006033.2, NONRATT006034.2 and NONRATT006035.2) could be compatible with their role in myocardial protection by stimulating their co-located gene (STAT3) after hemorrhagic shock and resuscitation. The final prognosis of I/R injury might be regulated by different genes, which is regarded as a complex network.

中文翻译：

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通过大鼠模型中的RNA测序分析严重失血性休克和复苏后心肌长非编码RNA和mRNA的长时程变化。

缺血再灌注损伤已被证明可导致器官功能障碍和死亡，尽管其机理尚不完全清楚。长的非编码RNA（lncRNA）在某些生物过程和疾病（包括心肌缺血再灌注（I / R）损伤）的基因表达中的重要作用已引起广泛关注。本文共将26只Sprague-Dawley（SD）大鼠随机分为两组：假手术和缺血再灌注（I / R）损伤。出血性休克是通过去除估计总血容量的45％，然后重新注入流血引起的。高通量RNA测序用于分析再灌注后4 h心脏组织中的差异表达（DE）lncRNA和信使RNA（mRNA）。还评估了心肌功能。复苏后 以心输出量，射血分数和心肌性能指数（MPI）表示的休克动物心肌功能的下降是显着的（p <0.05）。通过倍数变化的绝对值≥2和错误发现率≤0.001鉴定DE lncRNA和mRNA。与假手术组相比，在I / R损伤组的大鼠中，851个lncRNA和1015 mRNA显着上调，而1533个lncRNA和1702 m RNA显着下调。在DE lncRNA中，我们发现了12个与一些已知的凋亡相关蛋白编码基因相关的位置，这些基因相应地被上调或下调，包括STAT3和Il1r1。实时PCR分析证实了五种与位置相关的lncRNA（NONRATT006032.2，NONRATT006033.2，NONRATT006034.2，NONRATT006035.2和NONRATT029969）的表达水平。2）与假手术组相比，I / R损伤组大鼠中它们的位置相关mRNA（STAT3和Il1r1）均明显上调。DE lncRNAs（NONRATT006032.2，NONRATT006033.2，NONRATT006034.2和NONRATT006035.2）可以通过在失血性休克和复苏后刺激共同定位的基因（STAT3）来与其在心肌保护中的作用兼容。I / R损伤的最终预后可能受到不同基因的调节，这被认为是一个复杂的网络。2）可以通过在失血性休克和复苏后刺激其共同定位的基因（STAT3）来与其在心肌保护中的作用兼容。I / R损伤的最终预后可能受到不同基因的调控，这被认为是一个复杂的网络。2）通过在失血性休克和复苏后刺激其共同定位的基因（STAT3），可能与其在心肌保护中的作用相适应。I / R损伤的最终预后可能受到不同基因的调控，这被认为是一个复杂的网络。