title: Effects of Psoraleae fructus and its major component psoralen on Th2 response in allergic asthma.
abstract: This study is aimed to evaluate the effects of Psoraleae fructus (PF) on Th2 responses in a rat model of asthma in vivo and psoralen, a major constituent in PF, on Th2 responses in vitro. A rat model of asthma was established by sensitization and challenged with ovalbumin (OVA). Airway hyperresponsiveness was detected by direct airway resistance analysis. Lung tissues were examined for cell infiltration and mucus hypersecretion. Bronchoalveolar lavage fluid (BALF) was assessed for cytokine levels. In vitro study, Th2 cytokine production was evaluated in the culture supernatant of D10.G4.1 (D10 cells) followed by the determination of cell viability, meanwhile Th2 transcription factor GATA-3 expression in D10 cells was also determined. The oral administration of PF significantly reduced airway hyperresponsiveness (AHR) to aerosolized methacholine and decreased IL-4 and IL-13 levels in the BALF. Histological studies showed that PF markedly inhibited inflammatory infiltration and mucus secretion in the lung tissues. In vitro study, psoralen significantly suppressed Th2 cytokines of IL-4, IL-5 and IL-13 by ConA-stimulated D10 cells without inhibitory effect on cell viability. Furthermore, GATA-3 protein expression was also markedly reduced by psoralen. This study demonstrated that PF exhibited inhibitory effects on hyperresponsiveness and airway inflammation in a rat model of asthma, which was associated with the suppression of Th2 response. Psoralen, a major constituent of PF, has immunomodulatory properties on Th2 response in vitro, which indicated that psoralen might be a critical component of PF for its therapeutic effects.
authors.affiliation: Department of Respiratory Diseases, Hangzhou First People's Hospital of Zhejiang Province, Nanjing Medical University, Hangzhou 310006, Zhejiang Province, China , Institute of Integrated Traditional Chinese and Western Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China.
authors.forename: Hualiang
authors.initials: H
authors.lastname: Jin
authors.forename: Limin
authors.initials: L
authors.lastname: Wang
authors.forename: Changqing
authors.initials: C
authors.lastname: Xu
authors.forename: Bei
authors.initials: B
authors.lastname: Li
authors.forename: Qingli
authors.initials: Q
authors.lastname: Luo
authors.forename: Jinfeng
authors.initials: J
authors.lastname: Wu
authors.forename: Yubao
authors.initials: Y
authors.lastname: Lv
authors.forename: Genfa
authors.initials: G
authors.lastname: Wang
authors.forename: Jingcheng
authors.initials: J
authors.lastname: Dong
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents; D001249:Asthma / Q000188:drug therapy / Q000276:immunology* / Q000503:physiopathology; D016535:Bronchial Hyperreactivity / Q000188:drug therapy; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000276:immunology; D002478:Cells, Cultured; D016207:Cytokines / Q000032:analysis; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D005363:Ficusin / Q000302:isolation & purification / Q000494:pharmacology*; D018836:Inflammation Mediators / Q000032:analysis; D008297:Male; D010047:Ovalbumin / Q000276:immunology; D008517:Phytotherapy; D029907:Psoralea / Q000737:chemistry*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013047:Specific Pathogen-Free Organisms; D018418:Th2 Cells / Q000276:immunology*
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D018836:Inflammation Mediators; D010047:Ovalbumin; D005363:Ficusin