Σφακιανάκης Αλέξανδρος
ΩτοΡινοΛαρυγγολόγος
Αναπαύσεως 5 Άγιος Νικόλαος
Κρήτη 72100
00302841026182
00306932607174
alsfakia@gmail.com

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Σάββατο 15 Ιουλίου 2017

Regulatory effect of baicalin on the imbalance of Th17/Treg responses in mice with allergic asthma

Publication date: 17 August 2017
Source:Journal of Ethnopharmacology, Volume 208
Author(s): Lu Xu, Jinxia Li, Yu Zhang, Peng Zhao, Xuemei Zhang
Ethnopharmacology relevanceBaicalin, a flavonoid compound, was isolated from traditional Chinese medicine Scutellaria baicalensis Georgi. The study aimed to explore the regulatory effect of baicalin on immunological balance of Th17/Treg responses and the possible mechanisms in mice with allergic asthma.Materials and methodsMice were sensitized and challenged with OVA+LPS by intranasal instillation, and were intragastrically treated with baicalin from days 22–36 after sensitization. The organ coefficient of lung was determined. Immunoglobulin E (IgE) level in serum and cytokine IL-17A, IL-6, IL-10 levels in bronchoalveolar lavage fluid (BALF) were measured by ELISA. Histological changes in lung and airway tissues were observed by hematoxylin and eosin (H&E) and periodic acid-Schiff staining (PAS). The expressions of signal transducer and activator of transcription 3 (STAT3) and forkhead box P3 (FOXP3) in lung tissues were evaluated by immunohistochemistry and western blot methods.ResultsBaicalin obviously decreased OVA+LPS-induced organ coefficient of lung, inhibited serum IgE and BALF IL-7A and IL-6 secrection, promoted BALF IL-10 secrection in a dose-dependent manner. Histological studies demonstrated that baicalin significantly alleviated OVA+LPS-induced inflammatory responses and mucus secretion in lung and airway tissues. Immunohistochemistry and western blot studies showed that baicalin substantially suppressed STAT3 expression and promoted FOXP3 expression in lung tissues of mice.ConclusionsThese findings suggest that baicalin effectively protects against OVA+LPS-induced allergic asthma in mice by regulating the immunological imbalance of Th17/Treg responses.

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