miR-141-3p通过准SUGT1来抑制结肠上皮细胞热致死来缓解性结肠炎
Rong Yan1, Xinghua Liang1, Juan Hu1
1The Fourth Affiliated Hospital of Guangzhou Medical University (Zengcheng District people's Hospital of Guangzhou).
微RNA-141-3p通过向SUGT1.1,抑制结肠上皮细胞中的热致死,并缓解性结肠炎 (UC). 这一发现表明miR-141-3p作为治疗UC的潜在治疗性核酸药物.
科学领域:
- 胃肠病学 胃肠病学
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 性结肠炎 (UC) 是一种慢性炎症性结肠疾病.
- 结肠上皮细胞的灭与UC发育和进展密切相关.
- 微RNAs (miRNAs) 涉及UC和热致死.
研究的目的:
- 确定抑制结肠上皮细胞中 pyroptosis 的特定miRNAs.
- 研究这些miRNAs在UC治疗中的治疗潜力.
主要方法:
- 在FHC细胞中诱导炎症使用脂多糖 (LPS) 模拟肠炎.
- 通过各种测试 (CCK-8,流细胞计,ELISA,qPCR,西部斑点,免疫光) 检测到烧灭症指标.
- 使用生物信息学 (miRDB,TargetScan,KEGG) 和双露西法酶试验预测和验证的miRNA目标.
- 在小鼠DSS结肠炎模型中评估miR-141-3p的影响.
主要成果:
- 在LPS诱导的FHC细胞中,miR-141-3p被显著降低.
- miR-141-3p促进了FHC细胞的增殖,并抑制了亡和热亡.
- miR-141-3p降低了与热致死相关的蛋白质 (NLRP3,caspase-1,N-GSDMD) 和炎症性细胞因子 (IL-18,IL-1β).
- miR-141-3p准了SUGT1,抑制了热致死;SUGT1的过度表达恢复了抑制,而敲击则逆转了它.
- 在小鼠DSS模型中,miR-141-3p减轻了结肠炎症状.
结论:
- miR-141-3p通过准SUGT1.1,抑制LPS诱导的结肠上皮细胞中的烧灭.
- miR-141-3p在小鼠中显示出缓解DSS诱导的大肠炎的治疗潜力.
- miR-141-3p可能作为治疗性结肠炎的新型核酸药物.
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