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本文引用的文献

1
Antiasthmatic effects of hesperidin, a potential Th2 cytokine antagonist, in a mouse model of allergic asthma.橙皮苷作为潜在的 Th2 细胞因子拮抗剂对过敏性哮喘小鼠模型的平喘作用。
Mediators Inflamm. 2011;2011:485402. doi: 10.1155/2011/485402. Epub 2011 May 4.
2
What is the lifetime risk of physician-diagnosed asthma in Ontario, Canada?在加拿大安大略省,医生诊断的哮喘的终生风险是多少?
Am J Respir Crit Care Med. 2010 Feb 15;181(4):337-43. doi: 10.1164/rccm.200907-1035OC. Epub 2009 Nov 19.
3
Protein tyrosine phosphatases regulate asthma development in a murine asthma model.蛋白酪氨酸磷酸酶在小鼠哮喘模型中调节哮喘的发展。
J Immunol. 2009 Feb 1;182(3):1334-40. doi: 10.4049/jimmunol.182.3.1334.
4
GATA3 and the T-cell lineage: essential functions before and after T-helper-2-cell differentiation.GATA3与T细胞谱系:辅助性T细胞2细胞分化前后的重要功能
Nat Rev Immunol. 2009 Feb;9(2):125-35. doi: 10.1038/nri2476.
5
Imiquimod, a toll-like receptor 7 ligand, inhibits airway remodelling in a murine model of chronic asthma.咪喹莫特,一种Toll样受体7配体,在慢性哮喘小鼠模型中抑制气道重塑。
Clin Exp Pharmacol Physiol. 2009 Jan;36(1):43-8. doi: 10.1111/j.1440-1681.2008.05027.x. Epub 2008 Aug 26.
6
Mitochondrial structural changes and dysfunction are associated with experimental allergic asthma.线粒体结构变化和功能障碍与实验性变应性哮喘相关。
J Immunol. 2008 Sep 1;181(5):3540-8. doi: 10.4049/jimmunol.181.5.3540.
7
Interleukin 17-producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages.产生白细胞介素17的CD4+效应T细胞通过不同于1型和2型辅助性T细胞谱系的途径发育。
Nat Immunol. 2005 Nov;6(11):1123-32. doi: 10.1038/ni1254. Epub 2005 Oct 2.
8
Targeting memory Th2 cells for the treatment of allergic asthma.靶向记忆性Th2细胞治疗过敏性哮喘。
Pharmacol Ther. 2006 Jan;109(1-2):107-36. doi: 10.1016/j.pharmthera.2005.06.006. Epub 2005 Aug 2.
9
The global burden of asthma: executive summary of the GINA Dissemination Committee report.哮喘的全球负担:全球哮喘防治创议传播委员会报告执行摘要
Allergy. 2004 May;59(5):469-78. doi: 10.1111/j.1398-9995.2004.00526.x.
10
The function role of GATA-3 in Th1 and Th2 differentiation.GATA-3在Th1和Th2细胞分化中的功能作用。
Immunol Res. 2003;28(1):25-37. doi: 10.1385/IR:28:1:25.

在哮喘小鼠模型中,乳香酸通过抑制pSTAT6下调GATA3来减轻哮喘表型。

Boswellic acid attenuates asthma phenotypes by downregulation of GATA3 via pSTAT6 inhibition in a murine model of asthma.

作者信息

Liu Zhimin, Liu Xiaoyun, Sang Lili, Liu Haifeng, Xu Qinghua, Liu Zhehui

机构信息

Department of Cadre Health Protection, Liaocheng People's Hospital Liaocheng 252000, China.

出版信息

Int J Clin Exp Pathol. 2015 Jan 1;8(1):236-43. eCollection 2015.

PMID:25755710
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4348891/
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.

摘要

哮喘是一个严重的全球性健康问题,其特征为气道炎症、气道上皮壁脱落、黏液分泌增加、免疫球蛋白E(IgE)水平升高以及气道高反应性。哮喘的病理生理学由产生白细胞介素-4、白细胞介素-5、白细胞介素-13和白细胞介素-9等Th2细胞因子的Th2细胞介导。Th2细胞的分化由转录因子GATA3诱导,而GATA3通过IL-4信号传导被磷酸化信号转导及转录激活因子6(pSTAT6)激活。为了研究乳香酸的抗哮喘潜力及其潜在机制,我们在哮喘小鼠模型中研究了其抗哮喘潜力。在本研究中,BALB/c小鼠经卵清蛋白(OVA)全身致敏,随后进行雾化过敏原激发。我们在哮喘小鼠模型中研究了乳香酸对气道高反应性、炎性细胞浸润、Th2细胞因子和OVA特异性IgE产生的影响。我们发现,乳香酸治疗组抑制了过敏性气道炎症、气道高反应性、OVA特异性IgE和Th2细胞因子的分泌。它还以剂量依赖的方式抑制了pSTAT6和GATA3的表达。我们的数据表明,乳香酸有效治疗哮喘的机制是通过抑制pSTAT6和GATA-3的表达来减少Th2细胞因子。