Huang Wei Min, Liang Yong Qi, Tang Li Jun, Ding Yue, Wang Xiao Hong
Department of Neonatology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.
Exp Ther Med. 2013 Jul;6(1):199-203. doi: 10.3892/etm.2013.1074. Epub 2013 Apr 23.
The aim of this study was to explore the role of astragalus polysaccharide (APS) in the pathogenesis of bronchopulmonary dysplasia (BPD) in preterm children using an established BPD cell model. EA.hy926 cell cultures were divided into three groups: the air group as the blank control, the hyperoxia group as the experimental control and the APS group (2.5 mg/ml). The production of superoxide dismutase (SOD), malondialdehyde (MDA) and reactive oxygen species (ROS) were analyzed by biochemical assays. Real-time reverse transcription-polymerase chain reaction (RT-PCR) and western blotting were used to detect the RNA and protein expression levels of inflammatory cytokines, including interleukin (IL)-8, intercellular adhesion molecule 1 (ICAM-1) and nuclear factor (NF)-κB p65. Compared with the hyperoxia group, the ROS and MDA levels of the APS group were significantly reduced. By contrast, SOD production was significantly increased. The expression of IL-8, ICAM-1 and NF-κB p65 in the APS group was downregulated. APS acts as an antioxidant by stimulating SOD production while inhibiting lipid peroxidation in the EA.hy926 cells. Furthermore, this study demonstrated that APS retards the inflammatory response, as shown by the reduced expression of NF-κB p65, IL-8 and ICAM-1 when APS was added.
本研究旨在利用已建立的支气管肺发育不良（BPD）细胞模型，探讨黄芪多糖（APS）在早产儿支气管肺发育不良发病机制中的作用。将EA.hy926细胞培养物分为三组：空气组作为空白对照，高氧组作为实验对照，APS组（2.5mg/ml）。通过生化分析检测超氧化物歧化酶（SOD）、丙二醛（MDA）和活性氧（ROS）的产生。采用实时逆转录-聚合酶链反应（RT-PCR）和蛋白质印迹法检测炎症细胞因子的RNA和蛋白质表达水平，包括白细胞介素（IL）-8、细胞间黏附分子1（ICAM-1）和核因子（NF）-κB p65。与高氧组相比，APS组的ROS和MDA水平显著降低。相反，SOD的产生显著增加。APS组中IL-8、ICAM-1和NF-κB p65的表达下调。APS通过刺激EA.hy926细胞中SOD的产生，同时抑制脂质过氧化作用，起到抗氧化剂的作用。此外，本研究表明，当添加APS时，NF-κB p65、IL-8和ICAM-1的表达降低，表明APS可延缓炎症反应。
