title: Baicalin Alleviates Silica-Induced Lung Inflammation and Fibrosis by Inhibiting the Th17 Response in C57BL/6 Mice.
abstract: Silicosis is an inflammatory and fibrotic lung disease caused by inhalation of silica. Th17 cells play a key role in causing silica-induced lung inflammation and fibrosis. Baicalin, a compound isolated from the Chinese herb Huangqin, could suppress the differentiation of Th17 cells and alleviate inflammation. However, there are very few reports of the immunoregulatory mechanisms of baicalin in experimental silica-induced lung inflammation and fibrosis. In our study, mice were exposed to silica by intratracheal instillation, and in this way we established an experimental silicosis model. To elucidate the effects and mechanisms of baicalin in silica-induced inflammation and fibrosis, we used baicalin to treat the developed mouse model of silicosis. Treatment with baicalin attenuated the accumulation of inflammatory cells and led to milder pathological inflammatory and fibrotic changes in lung tissues. Baicalin affected the immunological balance between Th17 and Treg responses. Therefore, baicalin caused a decrease in Th17 cells by stimulating Treg cells and by inhibiting IL-6 and IL-23. We further demonstrated that silica-induced Th1 and Th2 immune responses were both inhibited by increased Treg activation, which was promoted by baicalin. Our findings confirmed the potential functions of baicalin in inhibiting the Th17 response and reducing silica-induced inflammation and fibrosis.
authors.affiliation: Department of Occupational and Environmental Health, School of Public Health, and ‡Department of Natural Products Chemistry, School of Pharmacy, China Medical University , Shenyang 110122, People's Republic of China.
authors.forename: Tao
authors.initials: T
authors.lastname: Liu
authors.affiliation: Department of Occupational and Environmental Health, School of Public Health, and ‡Department of Natural Products Chemistry, School of Pharmacy, China Medical University , Shenyang 110122, People's Republic of China.
authors.forename: Wujing
authors.initials: W
authors.lastname: Dai
authors.affiliation: Department of Occupational and Environmental Health, School of Public Health, and ‡Department of Natural Products Chemistry, School of Pharmacy, China Medical University , Shenyang 110122, People's Republic of China.
authors.forename: Chao
authors.initials: C
authors.lastname: Li
authors.affiliation: Department of Occupational and Environmental Health, School of Public Health, and ‡Department of Natural Products Chemistry, School of Pharmacy, China Medical University , Shenyang 110122, People's Republic of China.
authors.forename: Fangwei
authors.initials: F
authors.lastname: Liu
authors.affiliation: Department of Occupational and Environmental Health, School of Public Health, and ‡Department of Natural Products Chemistry, School of Pharmacy, China Medical University , Shenyang 110122, People's Republic of China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Chen
authors.affiliation: Department of Occupational and Environmental Health, School of Public Health, and ‡Department of Natural Products Chemistry, School of Pharmacy, China Medical University , Shenyang 110122, People's Republic of China.
authors.forename: Dong
authors.initials: D
authors.lastname: Weng
authors.affiliation: Department of Occupational and Environmental Health, School of Public Health, and ‡Department of Natural Products Chemistry, School of Pharmacy, China Medical University , Shenyang 110122, People's Republic of China.
authors.forename: Jie
authors.initials: J
authors.lastname: Chen
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D005419:Flavonoids / Q000737:chemistry / Q000494:pharmacology*; D007249:Inflammation / Q000139:chemically induced; D020381:Interleukin-17 / Q000276:immunology; D053583:Interleukin-1beta / Q000037:antagonists & inhibitors; D053759:Interleukin-23 / Q000037:antagonists & inhibitors; D008168:Lung / Q000503:physiopathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D015394:Molecular Structure; D011014:Pneumonia; D016133:Polymerase Chain Reaction; D031364:Scutellaria baicalensis / Q000737:chemistry; D012822:Silicon Dioxide / Q000494:pharmacology* / Q000633:toxicity; D012829:Silicosis / Q000503:physiopathology; D050378:T-Lymphocytes, Regulatory / Q000378:metabolism; D058504:Th17 Cells / Q000187:drug effects; D000093242:Interleukin-6 Inhibitors
chemical_list: D005419:Flavonoids; D020381:Interleukin-17; D053583:Interleukin-1beta; D053759:Interleukin-23; D012822:Silicon Dioxide; D000093242:Interleukin-6 Inhibitors; C038044:baicalin