氧化应激
炎症
医学
嗜酸性粒细胞
嗜酸性粒细胞趋化因子
免疫学
卵清蛋白
支气管肺泡灌洗
药理学
细胞因子
肺
趋化因子
哮喘
内分泌学
内科学
免疫系统
作者
Wen Cheng Huang,Tse-Hung Huang,Kuo Wei Yeh,Ya-Wen Chen,Szu Chuan Shen,Chian-Jiun Liou
标识
DOI:10.1016/j.jgr.2021.03.002
摘要
Ginsenoside Rg3, isolated from Panax ginseng , has anti-inflammatory and anti-tumor activities. It is known to reduce inflammation in acute lung injury in mice, and to reduce the expression of inflammatory cytokines and COX-2 in human asthmatic airway epithelium. In this study, we attempted to determine whether ginsenoside Rg3 inhibits airway inflammation, oxidative stress, and airway hyperresponsiveness (AHR) in the lungs of asthmatic mice. We also investigated its effects on oxidative stress and the inflammatory response in tracheal epithelial cells. Asthma symptoms were induced in female BALB/c mice sensitized with ovalbumin (OVA). Mice were divided into five groups: normal controls, OVA-induced asthmatic controls, and asthmatic mice treated with ginsenoside Rg3 or prednisolone by intraperitoneal injection. Inflammatory BEAS-2B cells (human tracheal epithelial cells) treated with ginsenoside Rg3 to investigate its effects on inflammatory cytokines and oxidative responses. Ginsenoside Rg3 treatment significantly reduced eosinophil infiltration, oxidative responses, airway inflammation, and AHR in the lungs of asthmatic mice. Ginsenoside Rg3 reduced Th2 cytokine and chemokine levels in bronchoalveolar lavage fluids and lung. Inflammatory BEAS-2B cells treated with ginsenoside Rg3 reduced the eotaxin and pro-inflammatory cytokine expressions, and monocyte adherence to BEAS-2B cells was significantly reduced as a result of decreased ICAM-1 expression. Furthermore, ginsenoside Rg3 reduced the expression of reactive oxygen species in inflammatory BEAS-2B cells. Ginsenoside Rg3 is a potential immunomodulator that can ameliorate pathological features of asthma by decreasing oxidative stress and inflammation • Ginsenoside Rg3 reduced eosinophil infiltration, and airway hyperresponsiveness in the lungs of asthmatic mice. • Ginsenoside Rg3 inhibited oxidative responses in the lungs. • Ginsenoside Rg3 reduced the levels of Th2 cytokines in BALF and lung. • Ginsenoside Rg3 inhibited monocyte cell adherence to tracheal epithelial cells. • Ginsenoside Rg3 reduced the levels of pro-inflammatory cytokines in tracheal epithelial cells.
科研通智能强力驱动
Strongly Powered by AbleSci AI