普兰托西亚尼丁B2通过PI3K/Akt/NFkB通路缓解LPS诱导的RAW264.7细胞炎症和氧化应激
Xiaoyan Ou1,2,3, Xin Chen1,2,3, Zhichun Fang1,2,3
1The Affiliated Stomatological Hospital, Jiangxi Medical College, Nanchang University, NO.688, Honggu North Road, Honggu Tan District, Nanchang City, 330038 Jiangxi Province China.
Cytotechnology
|March 13, 2025
概括
在牙周炎模型中,Proanthocyanidin B2 (PB2) 通过抑制PI3K/Akt/NFκB通路,有效地减少炎症和氧化应激. 这种天然化合物显示出治疗这种慢性炎症疾病的前景.
科学领域:
- 口腔生物学 口腔生物学
- 药理学 药理学是指药理学的学科.
- 免疫学 免疫学 免疫学
背景情况:
- 牙周炎是一种与全身疾病相关的慢性炎症性疾病.
- 一种聚醇的普兰托西亚尼丁B2 (PB2) 具有已知的抗炎和抗氧化特性.
- 关于PB2在牙周炎中的有效性和机制的研究有限.
研究的目的:
- 研究PB2的抗炎和抗氧化作用.
- 为了阐明PB2在Porphyromonas gingivalis LPS刺激细胞中的分子机制.
- 评估PB2对PI3K/Akt/NFκB信号通路的影响.
主要方法:
- 使用CCK-8试验评估了细胞活力.
- 炎症性细胞因子表达 (IL-1β,IL-6,TNF-α,IL-10) 通过qRT-PCR和ELISA进行测量.
- 评估了氧化应激标志物 (ROS,MDA,NO) 和抗氧化能力.
- 西方涂抹分析了PI3K/Akt/NFκB通路的激活.
主要成果:
- PB2显著降低了促炎性细胞因子 (IL-1β,IL-6,TNF-α) 和氧化应激标志物 (ROS,MDA,NO) 的调节.
- PB2增强了抗炎IL-10和总抗氧化能力.
- PB2 抑制了 PI3K/Akt/NFκB 信号通路的激活.
- 一种PI3K激动剂部分逆转了PB2的作用,证实了途径的参与.
结论:
- 在RAW264.7细胞中,PB2表现出强大的抗炎和抗氧化作用,对抗P. gingivalis LPS诱导的炎症.
- 该机制涉及PI3K/Akt/NFκB信号通路的抑制.
- PB2具有作为治疗牙周炎的治疗剂的潜力.
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