miR-34a/Notch1b mediated autophagy and apoptosis contributes to oxidative stress amelioration by emodin in the intestine of teleost Megalobrama amblycephala

文献类型： 外文期刊

第一作者： Song, Changyou

作者： Song, Changyou;Ge, Xianping;Li, Hongxia;Liu, Bo;Xu, Pao;Song, Changyou;Liu, Bo;Ge, Xianping;Li, Hongxia;Liu, Bo;Xu, Pao;Liu, Bo;Ge, Xianping;Li, Hongxia;Liu, Bo;Xu, Pao

作者机构：

关键词： Oxidative stress; miR-34a; Notch1b; Autophagy; Apoptosis; Emodin; Megalobrama amblycephala

期刊名称：AQUACULTURE （ 影响因子：5.135； 五年影响因子：5.125 ）

ISSN： 0044-8486

年卷期： 2022 年 547 卷

页码：

收录情况： SCI

摘要： Stress stimulated reactive oxygen species (ROS) excessive accumulation is the principal cause of oxidative damage in aquatic animals. Severe oxidative stress could induce cell fate dysfunction, affect physiologic derangement, growth, and even survival. This study aims to investigate the ameliorative function of emodin in resist to oxidative stress via histomorphology, transcriptome, miRNAs, and mRNA-miRNA integrate analysis in the intestine of Megalobrama amblycephala. Morphologically, emodin alleviated oxidative stress induced autophagy in intestine. Differentially expressed miRNAs induced by oxidative stress and emodin were mainly involved in energy metabolism, oxidative homeostasis, cell apoptosis and cancerization signaling. Specifically, target prediction of miRNAs reveals Notch and apoptosis signaling were dysregulated. mRNA-miRNA integrated analysis reveals miR-34a and Notch1b were actively co-related in the regulatory network, and miR-34a was solidly confirmed as the negative regulator of Notch1b by targeting to the 3'-UTR. Transcriptional expression of key genes reveal emodin alleviates intestinal oxidative stress by activating miR-34a, and subsequently inhibit the expression of Notch receptors (DllA, Jag1b, and Jag2) and down-stream regulators (Hes1, Hey1, and FBW7). Meanwhile, apoptosis-related gene expression (Bax, Casp3, Casp8, Casp9, AIF1, AIF3, CytoC, and CDK4) were activated by oxidative stress, while were alleviated to the control level when treated with emodin. In conclusion, these results suggest that miR-34a/Notch1b is the potential therapeutic target for emodin to ameliorate oxidative stress in M. amblycephala.

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