奥莱阿诺酸通过抑制c-Jun和MAPK通路来减弱IPEC-J2细胞的过氧化诱导的亡
Mingyang Hu1, Lei Zhang1, Hongpeng Jia1
1Laboratory of Molecular Nutrition and Immunity, College of Animal Science and Technology, Northeast Agricultural University, Harbin, People's Republic of China.
Journal of biochemical and molecular toxicology
|September 14, 2023
概括
醇酸 (OA) 通过减少亡来保护肠道细胞免受氧化应激. 它通过降低c-Jun和MAPK信号通路的调节来实现这一目标,为肠道疾病提供治疗潜力.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 烯酸 (OA) 是一种具有广泛治疗潜力的天然三烯酸.
- 甲状腺炎影响肠道上皮细胞中压力诱导的亡的确切机制尚未完全理解.
- 肠上皮细胞易受氧化应激的影响,这可能导致细胞亡和疾病.
研究的目的:
- 调查酸 (OA) 对肠道上皮细胞中氧化应激的保护作用.
- 在氧化应激模型中阐明OA作用的潜在分子机制.
- 确定OA对压力诱导的亡和相关信号通路的影响.
主要方法:
- 在IPEC-J2肠道细胞中使用过氧化 (H2O2) 创建了氧化应激的体外模型.
- 用RNA测序进行基因表达分析.
- 使用定量实时聚合酶连锁反应 (qRT-PCR) 和西部斑点分析来验证基因和蛋白质表达水平.
主要成果:
- 烯酸 (OA) 显示了肠道细胞中H2O2诱导的亡的度依赖减弱.
- RNA测序和途径分析表明,OA通过通过MAPK信号途径降低基因表达的调节来减轻H2O2细胞毒性.
- 西方斑点分析证实,OA抑制了c-Jun蛋白的H2O2诱导的表达.
结论:
- 烯酸 (OA) 预处理显著保护肠道上皮细胞免受H2O2诱导的亡.
- 保护作用通过抑制c-Jun蛋白和MAPK信号通路进行介导.
- 氧化作为治疗治疗与氧化压力相关的肠道疾病的治疗剂具有前景.
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