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CAVO抑制卵清蛋白诱导的小鼠哮喘模型中的气道炎症和2型固有淋巴细胞

CAVO Inhibits Airway Inflammation and ILC2s in OVA-Induced Murine Asthma Mice.

作者信息

Huang Feng, Tong Xiaoyun, Hu Chunyan, Zhang Qiushi, Wei Yijie, Hu Min, Kong Lingqi, Fu Rongbing, Li Xiaohong, Xie Yuhuan, Ming Xi, Chen Bojun, Lin Yuping, Xiong Lei

机构信息

School of Chinese Materia Medica & Yunnan Key Laboratory of Southern Medicine Utilization, Yunnan University of Chinese Medicine, Kunming, China.

The First Affiliated Hospital of Yunnan University of Chinese Medicine, Yunnan University of Chinese Medicine, Kunming, China.

出版信息

Biomed Res Int. 2023 Jan 10;2023:8783078. doi: 10.1155/2023/8783078. eCollection 2023.

Abstract

Cang-ai volatile oil (CAVO) is an aromatic Chinese medicine and is widely used to treat upper respiratory tract infections in children. However, the mechanism of CAVO in asthma treatment is unclear. In this study, we investigated the effects of CAVO on airway inflammation and the mechanism of inhibiting Group-2 innate lymphoid cells (ILC2s) in asthmatic mice, which was induced with Ovalbumin (OVA). CAVO improved AHR and airway inflammation in asthmatic mice. CAVO reduced the production of interleukin (IL)-2, IL-4, IL-5, IL-6, IL-7, IL-9, IL-13, IL-25, IL-33, and thymic stromal lymphopoietin (TSLP) in the bronchoalveolar lavage fluid (BALF), while increased the production of IL-10, significantly. CAVO also inhibited the suppressor of tumorigenicity 2 (ST2) and IL-33 expressions in the lung tissue. Moreover, flow analyses demonstrated that CAVO inhibited ILC2s activation by reducing the sedimentation of its upstream cytokines, thus alleviating downstream cytokines. This could be because of the downregulated microRNA-155 and upregulated microRNA-146a. CAVO inhibits ILC2s activation, thus further attenuating airway inflammation and AHR in asthmatic mice. These effects may be related to the downregulation of microRNA-155 and upregulation of microRNA-146a.

摘要

苍术挥发油(CAVO)是一种芳香类中药,广泛用于治疗儿童上呼吸道感染。然而,CAVO治疗哮喘的机制尚不清楚。在本研究中,我们探讨了CAVO对卵清蛋白(OVA)诱导的哮喘小鼠气道炎症的影响以及抑制2型固有淋巴细胞(ILC2s)的机制。CAVO改善了哮喘小鼠的气道高反应性(AHR)和气道炎症。CAVO降低了支气管肺泡灌洗液(BALF)中白细胞介素(IL)-2、IL-4、IL-5、IL-6、IL-7、IL-9、IL-13、IL-25、IL-33和胸腺基质淋巴细胞生成素(TSLP)的产生,同时显著增加了IL-10的产生。CAVO还抑制了肺组织中致瘤性2抑制因子(ST2)和IL-33的表达。此外,流式分析表明,CAVO通过减少其上游细胞因子的沉降来抑制ILC2s的激活,从而减轻下游细胞因子的产生。这可能是由于微小RNA-155下调和微小RNA-146a上调所致。CAVO抑制ILC2s的激活,从而进一步减轻哮喘小鼠的气道炎症和AHR。这些作用可能与微小RNA-155的下调和微小RNA-146a的上调有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7262/11401656/c98617adeac6/BMRI2023-8783078.001.jpg

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