Biochanin A 减轻城市颗粒物造成的氧化损伤。
摘要来源：Food Funct。 2021 年 3 月 15 日；12(5)：1958-1972。 PMID：33496707
摘要作者：薛朝晖、高鑫、余万丛、张谦、宋伟辰、李世豪、徐峥、寇晓红
文章单位：薛朝晖
摘要：城市颗粒物（UPM）是一种吸收空气污染物的有毒物质，可以进入肺泡，导致肺部疾病。研究表明，UPM的水溶性成分（WS-UPM）含有主要有毒物质，可引起肺细胞氧化损伤。在本研究中，通过仪器分析检测 UPM 颗粒尺寸和成分。鹰嘴豆中的异黄酮（生物鸡素 A (BCA)、芒柄花素和大豆黄酮）具有生物抗氧化特性。本研究旨在探讨其机制the oxidative damage induced by WS-UPM, and the protective role of isoflavones in human alveolar basal epithelial cells. The antioxidant activity of BCA, formononetin and daidzein was investigated through the total reduction capacity, diphenylpicrylhydrazine radical (DPPH), superoxide radical, and hydroxyl radical scavenging capacity detection. We also established cell models in vitro to further explore the BCA-protective mechanism. BCA presented a significant protection, and increased the levels of antioxidant makers including superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH). The effects were also reflected as the reduction of malondialdehyde (MDA) and nitric oxide (NO).此外，从RT-PCR和Western印迹技术获得的结果表明，MEK5/ERK5在调节BCA的抗氧化作用方面起着必不可少的作用，从而减轻了WS-UPM诱导的肺损伤。 Furthermore, BCA mitigated WS-UPM-exposed damage through upregulating the Nrf2 signaling pathway增强 Nrf2 下游抗氧化酶的表达。总之，我们的研究结果表明，WS-UPM 诱导的肺部疾病与氧化应激和 MEK5/ERK5-Nrf2 信号通路有关，BCA 通过上调 MEK5/ERK5-Nrf2 来调节 WS-UPM 诱导的肺损伤途径。