Shan Feng1, Erhong Duan2, Xiaojuan Shi3, Huiran Zhang4, Haitao Li4, Yunxia Zhao3, Lingshan Chao4, Xiaoqian Zhong5, Weiwei Zhang2, Rongqin Li6, Xixin Yan7. 1. Department of Respiratory and Critical Care Medicine, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China; Department of General Medicine, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, China. 2. School of Environmental Science and Engineering, Hebei University of Science and Technology, Shijiazhuang, Hebei 050018, China. 3. Department of Respiratory Medicine, The Third Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, China. 4. Department of Respiratory and Critical Care Medicine, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China. 5. Shijiazhuang Environmental Monitoring Center, Shijiazhuang, Hebei 050000, China. 6. Department of Central Laboratory, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China. 7. Department of Respiratory and Critical Care Medicine, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China. Electronic address: xi_xin_yan@126.com.
Abstract
BACKGROUND: Ambient fine particulate matter (PM2.5) could induce lung injury. Aryl hydrocarbon receptor (AhR) is involved in the molecular mechanisms of prooxidative and pro-inflammatory effect of PM2.5. Molecular hydrogen has antioxidant properties. The protective effect and mechanism of hydrogen on PM2.5-induced lung injury remain unclear. OBJECTIVES: This study aimed to determine whether hydrogen could alleviate lung injury in a rat model of subacute exposure to concentrated ambient PM2.5, and explore the mechanism related to AhR. METHODS: Male Wastar rats were exposed to either concentrated ambient particles (CAPs) (diameter: ≤2.5 μm, average concentration: 1328 ± 730 μg/m3) or filtered air (FA) by nose-only inhalation (5 h/day, 5 days/week for 4 weeks). Hydrogen-treated rats inhaled 66.7% hydrogen from water electrolysis for 2 h after each exposure to CAPs or FA. RESULTS: CAPs inhalation induced lung injury, as demonstrated by pulmonary function decrease, histopathological damage, mucus hypersecretion [Periodic acid-Schiff (PAS) staining for mucins, immunohistochemistry and quantitative real-time PCR (RT-qPCR) for mucin 5AC (MUC5AC) expression], increased pro-inflammatory cytokines (TNF-α, IL-8 and IL-1β) and oxidative damage indexes [malondialdehyde (MDA) and 8-isoprostane F2α (8-iso-PG)]. While, hydrogen inhalation significantly alleviated the damages mentioned above. In addition, low expression of AhR in lung tissues determined by Western Blot was found after CAPs exposure, whereas hydrogen inhibited AhR decline induced by CAPs. CONCLUSIONS: High concentrations of hydrogen could ameliorate pulmonary dysfunction, airway mucus hypersecretion, oxidation damage, and inflammation response in rats exposed to concentrated ambient PM2.5. Additionally, hydrogen alleviates lung injury induced by PM2.5 possibly through AhR-dependent mechanisms.
BACKGROUND: Ambient fine particulate matter (PM2.5) could induce lung injury. Aryl hydrocarbon receptor (AhR) is involved in the molecular mechanisms of prooxidative and pro-inflammatory effect of PM2.5. Molecular hydrogen has antioxidant properties. The protective effect and mechanism of hydrogen on PM2.5-induced lung injury remain unclear. OBJECTIVES: This study aimed to determine whether hydrogen could alleviate lung injury in a rat model of subacute exposure to concentrated ambient PM2.5, and explore the mechanism related to AhR. METHODS: Male Wastar rats were exposed to either concentrated ambient particles (CAPs) (diameter: ≤2.5 μm, average concentration: 1328 ± 730 μg/m3) or filtered air (FA) by nose-only inhalation (5 h/day, 5 days/week for 4 weeks). Hydrogen-treated rats inhaled 66.7% hydrogen from water electrolysis for 2 h after each exposure to CAPs or FA. RESULTS: CAPs inhalation induced lung injury, as demonstrated by pulmonary function decrease, histopathological damage, mucus hypersecretion [Periodic acid-Schiff (PAS) staining for mucins, immunohistochemistry and quantitative real-time PCR (RT-qPCR) for mucin 5AC (MUC5AC) expression], increased pro-inflammatory cytokines (TNF-α, IL-8 and IL-1β) and oxidative damage indexes [malondialdehyde (MDA) and 8-isoprostane F2α (8-iso-PG)]. While, hydrogen inhalation significantly alleviated the damages mentioned above. In addition, low expression of AhR in lung tissues determined by Western Blot was found after CAPs exposure, whereas hydrogen inhibited AhR decline induced by CAPs. CONCLUSIONS: High concentrations of hydrogen could ameliorate pulmonary dysfunction, airway mucus hypersecretion, oxidation damage, and inflammation response in rats exposed to concentrated ambient PM2.5. Additionally, hydrogen alleviates lung injury induced by PM2.5 possibly through AhR-dependent mechanisms.