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Siraitia grosvenorii Extract Attenuates Airway Inflammation in a Mouse Model of Respiratory Disease Induced by Particulate Matter 10 Plus Diesel Exhaust Particles
Sung, Y.-Y.; Kim, M.; Yuk, H.J.; Kim, S.-H.; Yang, W.-K.; Park, G.D.; Kim, K.S.; Ham, W.J.; Kim, D.-S. Siraitia grosvenorii Extract Attenuates Airway Inflammation in a Mouse Model of Respiratory Disease Induced by Particulate Matter 10 Plus Diesel Exhaust Particles. Nutrients2023, 15, 4140.
Sung, Y.-Y.; Kim, M.; Yuk, H.J.; Kim, S.-H.; Yang, W.-K.; Park, G.D.; Kim, K.S.; Ham, W.J.; Kim, D.-S. Siraitia grosvenorii Extract Attenuates Airway Inflammation in a Mouse Model of Respiratory Disease Induced by Particulate Matter 10 Plus Diesel Exhaust Particles. Nutrients 2023, 15, 4140.
Sung, Y.-Y.; Kim, M.; Yuk, H.J.; Kim, S.-H.; Yang, W.-K.; Park, G.D.; Kim, K.S.; Ham, W.J.; Kim, D.-S. Siraitia grosvenorii Extract Attenuates Airway Inflammation in a Mouse Model of Respiratory Disease Induced by Particulate Matter 10 Plus Diesel Exhaust Particles. Nutrients2023, 15, 4140.
Sung, Y.-Y.; Kim, M.; Yuk, H.J.; Kim, S.-H.; Yang, W.-K.; Park, G.D.; Kim, K.S.; Ham, W.J.; Kim, D.-S. Siraitia grosvenorii Extract Attenuates Airway Inflammation in a Mouse Model of Respiratory Disease Induced by Particulate Matter 10 Plus Diesel Exhaust Particles. Nutrients 2023, 15, 4140.
Abstract
Exposure to particulate matter (PM) causes considerable breathing-related health risks. We assessed the inhibitory effect of Siraitia grosvenorii extract (SGE) on airway inflammation in mice exposed to a fine dust mixture of PM10 (PM diameter < 10 mm) and diesel exhaust particles (DEPs) known as PM10D. SGE attenuated neutrophil infiltration and the number of immune B and T cells in lung tissue and bronchoalveolar lavage fluid (BALF) of PM10D-exposed mice. SGE reduced the secretion of cytokines and chemokines, including interleukin (IL)-1a, tumor necrosis factor (TNF)- a, IL-17, chemokine (C-X-C motif) ligand (CXCL)-1, and macrophage inflammatory protein (MIP)-2 in BALF. Airway inflammation, accumulation of inflammatory cells, and collagen fibrosis in the lung after PM10D exposure were investigated by histopathological analysis, and SGE treatment ameliorated these symptoms. SGE decreased the mRNA expression of mucin 5AC (MUC5AC), CXCL-1, TNF-a, MIP-2, and transient receptor potential vanilloid and ankyrin 1 ion channels in the lung tissues of mice. Furthermore, SGE ameliorated mitogen-activated protein kinase (MAPK)/nuclear factor-kappa B (NF-κB) signaling activated by PM10D in mice. We conclude that SGE attenuated PM10D-induced neutrophilic airway inflammation via inhibiting MAPK/NF-κB activation. These results show that SGE may be a candidate for the treatment of inflammatory respiratory diseases.
Medicine and Pharmacology, Pulmonary and Respiratory Medicine
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