由TNFα诱导的改变miRNA表达链接到子宫内膜异位症中NF-κB信号通路
Saswati Banerjee1, Wei Xu1, Aaron Doctor2
1Department of Physiology, Morehouse School of Medicine, Atlanta, GA, 30310, USA.
Inflammation
|June 30, 2023
概括
瘤坏死因子-α (TNFα) 在子宫内膜异位症中失调微RNA (miRNA),促进疾病的进展. 抗炎多曲素 (CUR) 通过抑制TNFα和相关信号通路来逆转这些效应.
科学领域:
- 妇科病理学的病理学
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- 子宫内膜异位症是一种常见的炎症性妇科疾病,与免疫系统失调有关.
- 瘤坏死因子-α (TNFα),一种强烈的炎症性细胞因子,与子宫内膜异位症的进展有关.
- 微RNAs (miRNAs) 在细胞功能中发挥作用,并可能参与子宫内膜异位症的发病.
研究的目的:
- 为了研究TNFα在调节失调miRNAs与NFkB信号通路在子宫内膜异位症相关的作用.
- 检查黄素 (CUR) 在调节TNFα诱导的miRNA变化和信号通路中的治疗潜力.
主要方法:
- 使用RT-qPCR在子宫内膜异位症患者 (EESC) 和正常子宫内膜层细胞 (NESC) 的原始细胞中量化miRNA表达.
- 用外源性TNFα对NESC进行治疗,以评估对miRNA表达的剂量依赖性影响.
- 西方斑分析用于测量NF-κB,PI3K,AKT和ERK信号通路的酸化.
- 评估黄素对miRNA表达和信号通路酸化的影响.
主要成果:
- 与NESC相比,在EESC中TNFα的升高显著降低了特定miRNA的调节.
- 对NESC的外源性TNFα治疗模仿了在EESC中观察到的miRNA下调.
- TNFα显著增加了PI3K,AKT,ERK和NF-κB信号通路的酸化.
- 库尔库明治疗剂量依赖于增加miRNA表达和抑制AKT,ERK和NF-κB酸化.
结论:
- 在子宫内膜异位症中,高调节的TNFα通过调节miRNA表达的失调,有助于疾病病理生理学.
- PI3K/AKT/ERK和NF-κB通路的TNFα激活与子宫内膜异位症的发病有关.
- 黄素通过抑制TNFα,恢复miRNA水平和抑制关键信号通路来证明其治疗潜力.
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