دورية أكاديمية

Baicalin attenuates LPS-induced alveolar type II epithelial cell A549 injury by attenuation of the FSTL1 signaling pathway via increasing miR-200b-3p expression

التفاصيل البيبلوغرافية
العنوان: Baicalin attenuates LPS-induced alveolar type II epithelial cell A549 injury by attenuation of the FSTL1 signaling pathway via increasing miR-200b-3p expression
المؤلفون: Xin-ya Duan, Yang Sun, Zhu-fen Zhao, Yao-qing Shi, Xun-yan Ma, Li Tao, Ming-wei Liu
المصدر: Innate Immunity, Vol 27 (2021)
بيانات النشر: SAGE Publishing, 2021.
سنة النشر: 2021
المجموعة: LCC:Immunologic diseases. Allergy
مصطلحات موضوعية: Immunologic diseases. Allergy, RC581-607
الوصف: In China, baicalin is the main active component of Scutellaria baicalensis , which has been used in the treatment of inflammation-related diseases, such as inflammation-induced acute lung injury. However, its specific mechanism remains unclear. This study examined the protective effect of baicalin on LPS-induced inflammation injury of alveolar epithelial cell line A549 and explored its protective mechanism. Compared with the LPS-induced group, the proliferation inhibition rates of alveolar type II epithelial cell line A549 intervened by different concentrations of baicalin decreased significantly, as did the levels of inflammatory factors IL-6, IL-1β, prostaglandin 2 and TNF-α in the supernatant. The expression levels of inflammatory proteins inducible NO synthase (iNOS), NF-κB65, phosphorylated ERK (p-ERK1/2), and phosphorylated c-Jun N-terminal kinase (p-JNK1) significantly decreased, as did the protein expression of follistatin-like protein 1 (FSTL1). In contrast, expression of miR-200b-3p significantly increased in a dose-dependent manner. These results suggested that baicalin could significantly inhibit the expression of inflammation-related proteins and improve LPS-induced inflammatory injury in alveolar type II epithelial cells. The mechanism may be related to the inhibition of ERK/JNK inflammatory pathway activation by increasing the expression of miR-200b-3p. Thus, FSTL1 is the regulatory target of miR-200b-3p.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1753-4259
1753-4267
17534259
Relation: https://doaj.org/toc/1753-4259; https://doaj.org/toc/1753-4267
DOI: 10.1177/17534259211013887
URL الوصول: https://doaj.org/article/db9021625e4e4f6f8d1cd01395b7273e
رقم الأكسشن: edsdoj.b9021625e4e4f6f8d1cd01395b7273e
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:17534259
17534267
DOI:10.1177/17534259211013887