title: The effects of cordycepin on ovalbumin-induced allergic inflammation by strengthening Treg response and suppressing Th17 responses in ovalbumin-sensitized mice.
abstract: The aim of the current study was to use a mouse model of allergic asthma to investigate whether cordycepin has antiasthmatic effects, and if so, to determine the mechanism of these effects. A total of 50 mice were randomly assigned to five experimental groups: control, model, dexamethasone (Dex, 2 mg/kg), and cordycepin (20-40 mg/kg). Histological studies were evaluated by the hematoxylin and eosin staining, OVA-specific serum and BALF IgE levels and Treg/Th17 cytokines were evaluated by enzyme-linked immunosorbent assay, and RORγt and Foxp3 were evaluated by western blot. Our study demonstrated that cordycepin inhibited OVA-induced increases in eosinophil count; IL-17A levels were recovered and increased IL-10 levels in bronchoalveolar lavage fluid. Histological studies demonstrated that cordycepin substantially inhibited OVA-induced eosinophilia in lung tissue. Western blot study demonstrated that cordycepin increased Foxp3 and inhibited RORγt. These findings suggest that cordycepin may effectively ameliorate the progression of asthma and could be used as a therapy for patients with allergic asthma.
authors.affiliation: College of Chinese Medicinal Materials, Jilin Agricultural University, Changhcun, 130118, China.
authors.forename: Zhang
authors.initials: Z
authors.lastname: Tianzhu
authors.forename: Yang
authors.initials: Y
authors.lastname: Shihai
authors.forename: Du
authors.initials: D
authors.lastname: Juan
mesh_terms: D000818:Animals; D018927:Anti-Asthmatic Agents / Q000627:therapeutic use*; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D001249:Asthma / Q000188:drug therapy*; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D003839:Deoxyadenosines / Q000627:therapeutic use*; D003907:Dexamethasone / Q000627:therapeutic use; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D004802:Eosinophilia / Q000188:drug therapy; D004804:Eosinophils / Q000276:immunology; D005260:Female; D051858:Forkhead Transcription Factors / Q000378:metabolism; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D007249:Inflammation / Q000188:drug therapy; D016753:Interleukin-10 / Q000378:metabolism; D020381:Interleukin-17 / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000378:metabolism; D010047:Ovalbumin; D011897:Random Allocation; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D058504:Th17 Cells / Q000276:immunology*
chemical_list: D018927:Anti-Asthmatic Agents; D000893:Anti-Inflammatory Agents; D003839:Deoxyadenosines; D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; C556062:IL10 protein, mouse; C098680:Il17a protein, mouse; D020381:Interleukin-17; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D016753:Interleukin-10; D007073:Immunoglobulin E; D003907:Dexamethasone; D010047:Ovalbumin; C058120:cordycepin