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提取物及其主要活性成分油酸通过抑制哮喘小鼠 Th2/GATA-3 和白细胞介素-17/RORγt 信号通路抑制卵清蛋白诱导的过敏性气道炎症。

Extract and Its Main Active Component, Oleic Acid, Inhibit Ovalbumin-Induced Allergic Airway Inflammation through Inhibition of Th2/GATA-3 and Interleukin-17/RORγt Signaling Pathways in Asthmatic Mice.

机构信息

Institute of Traditional Medicine & Bioscience, Daejeon University, Daejeon 34520, Korea.

Department of Herbology, College of Korean Medicine, Sangji University, 83 Sangjidae-gil, Wonju 26339, Korea.

出版信息

Molecules. 2021 Mar 25;26(7):1854. doi: 10.3390/molecules26071854.

Abstract

Cicadae Periostracum (CP), derived from the slough of , has been used as traditional medicine in Korea and China because of its diaphoretic, antipyretic, anti-inflammatory, antioxidant, and antianaphylactic activities. The major bioactive compounds include oleic acid (OA), palmitic acid, and linoleic acid. However, the precise therapeutic mechanisms underlying its action in asthma remain unclear. The objective of this study was to determine the antiasthmatic effects of CP in an ovalbumin (OVA)-induced asthmatic mouse model. CP and OA inhibited the inflammatory cell infiltration, airway hyperresponsiveness (AHR), and production of interleukin (IL)7 and Th2 cytokines (IL-5) in the bronchoalveolar lavage fluid and OVA-specific imunoglobin E (IgE) in the serum. The gene expression of IL-5, IL-13, CCR3, MUC5AC, and COX-2 was attenuated in lung tissues. CP and OA might inhibit the nuclear translocation of GATA-binding protein 3 (GATA-3) and retinoic acid receptor-related orphan receptor γt (RORγt) via the upregulation of forkhead box p3 (Foxp3), thereby preventing the activation of GATA-3 and RORγt. In the in vitro experiment, a similar result was observed for Th2 and GATA-3. These results suggest that CP has the potential for the treatment of asthma via the inhibition of the GATA-3/Th2 and IL-17/RORγt signaling pathways.

摘要

蝉蜕(CP)来源于蝉蜕,由于其具有发汗、解热、抗炎、抗氧化和抗过敏作用,已在韩国和中国被用作传统药物。主要的生物活性化合物包括油酸(OA)、棕榈酸和亚油酸。然而,其在哮喘中的作用的确切治疗机制尚不清楚。本研究旨在确定 CP 在卵清蛋白(OVA)诱导的哮喘小鼠模型中的抗哮喘作用。CP 和 OA 抑制了炎症细胞浸润、气道高反应性(AHR)以及支气管肺泡灌洗液中白细胞介素(IL)7 和 Th2 细胞因子(IL-5)和血清中 OVA 特异性免疫球蛋白 E(IgE)的产生。肺组织中 IL-5、IL-13、CCR3、MUC5AC 和 COX-2 的基因表达减弱。CP 和 OA 可能通过上调叉头框 P3(Foxp3)来抑制 GATA 结合蛋白 3(GATA-3)和维甲酸受体相关孤儿受体γt(RORγt)的核易位,从而防止 GATA-3 和 RORγt 的激活。在体外实验中,Th2 和 GATA-3 也观察到了类似的结果。这些结果表明,CP 通过抑制 GATA-3/Th2 和 IL-17/RORγt 信号通路,具有治疗哮喘的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c3ed/8037444/d2a344eaf1f1/molecules-26-01854-g001a.jpg

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