Hsieh Hsi-Lung, Liu Shih-Hai, Chen Ya-Ling, Huang Chien-Yi, Wu Shu-Ju
Department of Nursing, Division of Basic Medical Sciences, Research Center for Chinese Herbal Medicine, and Graduate Institute of Health Industry Technology, Chang Gung University of Science and Technology, Taoyuan City, Taiwan.
Department of Neurology, Chang Gung Memorial Hospital, Linkou, Taoyuan City, Taiwan.
Arch Physiol Biochem. 2022 Jun;128(3):757-766. doi: 10.1080/13813455.2020.1727525. Epub 2020 Feb 14.
Astragaloside IV isolated from (Fisch.), which was reported to have anti-tumor, anti-asthma, and suppressed cigarette smoke-induced lung inflammation in mice.
This study investigated whether astragaloside IV reduced the expression of inflammatory mediators and oxidative stress in BEAS-2B cells.
BEAS-2B cells treated with astragaloside IV, and then stimulated with TNF-α or TNF-α/IL-4. The levels of cytokine and chemokine were analysed with ELISA and real-time PCR.
Astragaloside IV significantly inhibited the levels of CCL5, MCP-1, IL-6 and IL-8. Astragaloside IV also reduced ICAM-1 expression for blocked THP-1 monocyte adhesion to BEAS-2B cells. Furthermore, astragaloside IV attenuated the phosphorylation of MAPK, and reduced the translocation of p65 into the nucleus. Astragaloside IV could increase the expression of HO-1 and Nrf2 for promoting the oxidant protective effect.
Aastragaloside IV has an anti-inflammatory and oxidative effect via regulated NF-κB, MAPK and HO-1/Nrf2 signalling pathways in human bronchial epithelial cells.
从黄芪中分离得到的黄芪甲苷IV据报道具有抗肿瘤、抗哮喘作用，并能抑制香烟烟雾诱导的小鼠肺部炎症。
本研究调查黄芪甲苷IV是否能降低BEAS-2B细胞中炎症介质的表达和氧化应激。
用黄芪甲苷IV处理BEAS-2B细胞，然后用TNF-α或TNF-α/IL-4刺激。用ELISA和实时PCR分析细胞因子和趋化因子水平。
黄芪甲苷IV显著抑制CCL5、MCP-1、IL-6和IL-8的水平。黄芪甲苷IV还降低了ICAM-1的表达，阻止THP-1单核细胞黏附于BEAS-2B细胞。此外，黄芪甲苷IV减弱了MAPK的磷酸化，并减少了p65向细胞核的转位。黄芪甲苷IV可增加HO-1和Nrf2的表达，促进抗氧化保护作用。
黄芪甲苷IV通过调节人支气管上皮细胞中的NF-κB、MAPK和HO-1/Nrf2信号通路发挥抗炎和抗氧化作用。
