Evidence from biochemical liver function index and histopathology analysis suggested that selenium could effectively repair the liver injury caused by beta-cypermethrin (β-CYP). However, the molecular mechanism of selenium against liver injury induced by β-CYP remains unclear. In the present study, dynamic changes in gene expression profiles before and after the treatment of Na₂SeO₃ in liver injury mice were analyzed by using RNA sequencing. As a result, several essential genes and pathways were identified to be significantly associated with this process. In particular, ten genes including Cyp2j11, Cyp2b10, Cyp3a13, Dhrs9, Socs2, Stat4, Gm13305, Cyp3a44, Retsat, and Cyp26b1 were significantly enriched in the functional categories related to retinol metabolism, linoleic acid metabolism, and Jak-STAT signaling pathway. Among them, the expression patterns of nine genes were validated by qRT-PCR, except for Cyp3a44. Furthermore, we have constructed the associated regulatory network based on the identified targets revealed by high throughput screening. Our study may provide insight into the molecular mechanism underlying the protective effect of selenium against liver injury induced by β-CYP in mammals.

中文翻译：

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硒通过RNA-seq对小鼠β-氯氰菊酯致肝损伤的转录组学研究。

从生化肝功能指数和组织病理学分析的证据表明，硒可以有效修复β-氯氰菊酯（β-CYP）引起的肝损伤。然而，硒对抗β-CYP肝损伤的分子机制尚不清楚。在本研究中，Na ₂ SeO ₃治疗前后基因表达谱的动态变化通过使用RNA测序来分析肝损伤中的小鼠。结果，确定了几个必不可少的基因和途径与该过程显着相关。特别是，包括Cyp2j11，Cyp2b10，Cyp3a13，Dhrs9，Socs2，Stat4，Gm13305，Cyp3a44，Retsat和Cyp26b1的十个基因在与视黄醇代谢，亚油酸代谢和Jak-STAT信号传导途径有关的功能类别中显着丰富。其中，除Cyp3a44外，通过qRT-PCR验证了9个基因的表达模式。此外，我们已经根据高通量筛选揭示的确定目标构建了相关的监管网络。我们的研究可能提供有关硒对哺乳动物中β-CYP所致肝损伤的保护作用的分子机制的见解。