Thioredoxin (Txn) is a hydrogen carrier protein and exists widely in organism. Txn deficiency implicates cardiomyocytes injury has been proven. However, the exact mechanism remains unclear. To understand the mechanistic response of cardiomyocytes subsequent to Txn suppression, we established the model of Txn dysfunction by employing gene interference technology (siRNA) and Txn inhibitor (PX‐12) in cardiomyocytes. We detected the ROS levels, inflammation factors, and key proteins in the autophagy and apoptosis. In addition, heat map was used for further analysis. Our results revealed that Txn dysfunction increased the release of ROS and induced activation of autophagy via upregulation of Becline‐1, LC3‐1, 2, which further regulated the inflammatory response, meanwhile, Txn silence inhibited apoptosis in chicken cardiomyocytes through Caspase‐3 inhibition. Altogether we concluded that Txn‐deficient chicken cardiomyocytes experienced autophagy, which caused severe inflammatory reactions and resulting in damage to cardiomyocytes.

中文翻译：

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硫氧还蛋白的功能障碍通过激活鸡心肌细胞的自噬引发炎症。

硫氧还蛋白（Txn）是一种氢载体蛋白，广泛存在于生物体内。已证明 Txn 缺乏与心肌细胞损伤有关。然而，确切的机制仍不清楚。为了了解Txn抑制后心肌细胞的机制反应，我们通过在心肌细胞中采用基因干扰技术（siRNA）和Txn抑制剂（PX-12）建立了Txn功能障碍模型。我们检测了自噬和细胞凋亡中的 ROS 水平、炎症因子和关键蛋白。此外，热图用于进一步分析。我们的研究结果表明，Txn 功能障碍通过上调 Becline-1、LC3-1、2 增加 ROS 的释放并诱导自噬激活，从而进一步调节炎症反应，同时，Txn 沉默通过 Caspase-3 抑制抑制鸡心肌细胞凋亡。总而言之，我们得出结论，Txn 缺陷的鸡心肌细胞经历了自噬，这会引起严重的炎症反应并导致心肌细胞受损。