The role of angiotensin II type 1 receptor (AT1R) in ultrafine particle-induced lung injury

• Main Authors: Wan-TingLin, 林婉婷
• Other Authors: Chih-Ching Chang
• Format: Others
• Language: zh-TW
• Published: 2015
• Online Access: http://ndltd.ncl.edu.tw/handle/99628908097145450902

碩士 === 國立成功大學 === 環境醫學研究所 === 103 === In this study, we investigated the role of angiotensin II type 1 receptor (AT1R) in ultrafine particle induced lung injury. Male ICR mice were oropharyngeal aspirated with ufCB (0, 100, 200 μg/mouse). For inhibitory study, a group of mice were injected with AT1R antagonist (ZD7155; 20 mg/kg) intraperitoneally 30 min before ufCB aspirated. The total cell counts, differential counts and total protein were measured in bronchoalveolar (BAL) fluid. Enzyme-linked immunosorbent assay (ELISA) was used to measure vascular endothelial growth factor (VEGF) and tumor necrosis factor alpha (TNF-α) in BAL fluid, and VEGF in blood. The results show that exposure to ufCB caused a dose-dependent increased the total cell counts, the numbers of neutrophils and total protein in BAL fluid, with the maximal increase at 21 hr. The data indicate that ufCB caused pulmonary inflammatory response and alveolar-capillary permeability. TNF-α was significantly increased at 6 hr. Furthermore, ufCB induced significant productions of VEGF in BAL fluid over the study period, with a maximal increase at 16 hr. Pretreatment with ZD7155 significantly reduced the total cell counts and neutrophils in BAL fluid. ZD7155 also reduced the expression of TNF-α, total protein and VEGF. The results from our study demonstrate that ufCB exposure induced pulmonary inflammatory response and alveolar-capillary permeability may be mediated by AT1R.