title: Boswellic acid attenuates asthma phenotypes by downregulation of GATA3 via pSTAT6 inhibition in a murine model of asthma.
abstract: Asthma is a serious global health problem characterised by airway inflammation, airway epithelial wall shedding, enhanced mucus production, increased IgE levels and airway hyperresponsiveness. The pathophysiology of asthma is mediated by Th2 cells which produce Th2 cytokines like interleukin-4, interleukin-5, interleukin-13 and interleukin-9. The differentiation of Th2 cells is induced by the transcription factor GATA3 which is activated by pSTAT6 via IL-4 signalling. To investigate the anti-asthmatic potential of Boswellic acid, as well as the underlying mechanism involved, we studied its anti-asthmatic potential in a murine model of asthma. In this study, BALB/c mice were systemically sensitized by ovalbumin (OVA) followed by aerosol allergen challenges. We investigated the effect of Boswellic acid on airway hyperresponsiveness, inflammatory cell infiltration, Th2 cytokine and OVA-specific IgE production in a mouse model of asthma. We found that Boswellic acid treated groups suppressed allergic airway inflammation, AHR, OVA-specific IgE and Th2 cytokines secretion. It also suppressed the expression of pSTAT6 and GATA3 in a dose dependent manner. Our data suggest that the mechanism by which Boswellic acid effectively treats asthma is based on reductions of Th2 cytokines via inhibition of pSTAT6 and GATA-3 expression.
authors.affiliation: Department of Cadre Health Protection, Liaocheng People's Hospital Liaocheng 252000, China.
authors.forename: Zhimin
authors.initials: Z
authors.lastname: Liu
authors.affiliation: Department of Cadre Health Protection, Liaocheng People's Hospital Liaocheng 252000, China.
authors.forename: Xiaoyun
authors.initials: X
authors.lastname: Liu
authors.affiliation: Department of Cadre Health Protection, Liaocheng People's Hospital Liaocheng 252000, China.
authors.forename: Lili
authors.initials: L
authors.lastname: Sang
authors.affiliation: Department of Cadre Health Protection, Liaocheng People's Hospital Liaocheng 252000, China.
authors.forename: Haifeng
authors.initials: H
authors.lastname: Liu
authors.affiliation: Department of Cadre Health Protection, Liaocheng People's Hospital Liaocheng 252000, China.
authors.forename: Qinghua
authors.initials: Q
authors.lastname: Xu
authors.affiliation: Department of Cadre Health Protection, Liaocheng People's Hospital Liaocheng 252000, China.
authors.forename: Zhehui
authors.initials: Z
authors.lastname: Liu
mesh_terms: D000818:Animals; D018927:Anti-Asthmatic Agents / Q000494:pharmacology*; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D001249:Asthma / Q000378:metabolism* / Q000473:pathology; D015153:Blotting, Western; D004195:Disease Models, Animal; D015536:Down-Regulation; D005260:Female; D050990:GATA3 Transcription Factor / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D010641:Phenotype; D050800:STAT6 Transcription Factor / Q000378:metabolism*; D014315:Triterpenes / Q000494:pharmacology*
chemical_list: D018927:Anti-Asthmatic Agents; D000894:Anti-Inflammatory Agents, Non-Steroidal; D050990:GATA3 Transcription Factor; C494748:Gata3 protein, mouse; D050800:STAT6 Transcription Factor; C494100:Stat6 protein, mouse; D014315:Triterpenes; C054625:boswellic acid
keywords: Asthma; GATA-3; IgE; Th2; airway hyperresponsiveness; eosinophil; pSTAT6