瑞可以减轻人体脂肪细胞中缺氧引起的炎症
Kathrin Geiger1,2, Axel Muendlein3, Andreas Leiherer3,4,5
1Vorarlberg Institute for Vascular Investigation and Treatment (VIVIT), Feldkirch, Austria. kathrin.geiger@vivit.at.
Molecular biology reports
|October 16, 2023
概括
植物化合物myricetin在氧气不足的情况下减少人体脂肪细胞的炎症. 它抑制了关键的炎症途径和阿迪波金表达,提供了潜在的抗炎益处.
科学领域:
- 生物化学 生化学
- 细胞生物学 细胞生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 脂肪组织缺氧有助于慢性炎症和与肥胖有关的疾病.
- 瑞是一种天然的黄类化合物,因其潜在的健康益处而闻名.
- 瑞对脂肪细胞中缺氧诱导的炎症途径的影响以前是未知的.
研究的目的:
- 为了研究瑞对缺氧诱导的炎症性阿迪波金和人类脂肪细胞中的通路的影响.
- 为了确定myricetin是否在低氧细胞模型中表现出抗炎作用.
主要方法:
- 差异化的人类SGBS脂肪细胞暴露于与或没有myricetin的诺莫西克和缺氧条件.
- 实时RT-PCR被用于测量阿迪波金基因表达.
- 西方斑点分析检测出了关键的转录因子 (HIF-1α,NF-κB,Akt,CREB,牛,slug).
主要成果:
- 瑞显著抑制了低氧诱导的阿迪波基因 (阿佩林,莱普丁,化学素,阿斯素,DPP-4) 的表达.
- 米瑞丁减少了HIF-1α的缺氧诱导的核积累.
- 瑞抑制了炎症调节剂NF-κB,Akt,CREB和前瘤原始因子Snail和Slug的激活.
结论:
- 瑞有效调节缺氧诱导的阿迪波金表达和人类脂肪细胞中的炎症途径.
- 这项研究提供了证据证明myricetin在缺氧挑战的人体脂肪细胞中的抗炎性质.
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