miRNAs are a class of small non‐coding RNAs that are involved in various biological processes. In the preliminary work of the laboratory, found that miR‐383‐5p was down‐regulated in the liver tissue of acute cold stress rats and has been shown to be an important regulatory factor in tumour proliferation, but there are very few studies involving the mediation of cold stress in rat liver tissues. Therefore, the purpose of this study was to determine the effect of miR‐383‐5p on the livers of cold stress rats by simulating the cold stress state of rat liver tissues in vitro using H₂O₂ to induce rat hepatocyte oxidative stress. The results showed that MDA content, Caspase 3 and Cyto C protein levels increased significantly; GPx activity and SOD1 protein levels decreased significantly and miR‐383‐5p expression was significantly down‐regulated in rat liver tissues after cold stress. Different concentrations of H₂O₂ was added to rat hepatocytes, and the results showed that the expression of miR‐383‐5p, the ROS level, and the apoptosis rate in rat hepatocytes was increased significantly in a concentration‐dependent fashion. Transfection of miR‐383‐5p inhibitor revealed that the apoptosis rate of rat hepatocytes, and the protein level of apoptosis‐related protein Caspase 3 were reduced; the results of the dual‐luciferase reporter gene assay showed that miR‐383‐5p targeted regulation of Bcl2. The results suggested that the expression of miR‐383‐5p was up‐regulated in oxidative stress rat hepatocytes and may aggravate the apoptosis of rat hepatocytes induced by targeting inhibition of Bcl2 translation.

中文翻译：

---

下调 miR-383-5p 通过靶向 Bcl2 抑制氧化应激大鼠肝细胞的凋亡。

miRNA是一类参与各种生物过程的小型非编码RNA。在实验室前期工作中，发现miR-383-5p在急性冷应激大鼠肝组织中表达下调，已被证明是肿瘤增殖的重要调节因子，但很少有研究涉及介导大鼠肝组织中的冷应激。_{因此，本研究的目的是通过使用H 2} O ₂在体外模拟大鼠肝组织的冷应激状态来确定miR-383-5p对冷应激大鼠肝脏的影响。诱导大鼠肝细胞氧化应激。结果表明，MDA含量、Caspase 3和Cyto C蛋白水平显着升高；冷应激后大鼠肝组织中 GPx 活性和 SOD1 蛋白水平显着降低，miR-383-5p 表达显着下调。不同浓度的H ₂ O ₂结果表明，大鼠肝细胞中 miR-383-5p 的表达、ROS 水平和凋亡率显着增加，呈浓度依赖性。转染miR-383-5p抑制剂后发现大鼠肝细胞凋亡率降低，凋亡相关蛋白Caspase 3蛋白水平降低；双荧光素酶报告基因检测结果表明 miR-383-5p 靶向调控 Bcl2。结果表明，miR-383-5p在氧化应激大鼠肝细胞中的表达上调，并可能加重靶向抑制Bcl2翻译诱导的大鼠肝细胞凋亡。