دورية أكاديمية

Dehydroabietic Acid Suppresses Inflammatory Response Via Suppression of Src-, Syk-, and TAK1-Mediated Pathways

التفاصيل البيبلوغرافية
العنوان: Dehydroabietic Acid Suppresses Inflammatory Response Via Suppression of Src-, Syk-, and TAK1-Mediated Pathways
المؤلفون: Eunji Kim, Young-Gyu Kang, Yong-Jin Kim, Tae Ryong Lee, Byong Chul Yoo, Minkyeong Jo, Ji Hye Kim, Jong-Hoon Kim, Donghyun Kim, Jae Youl Cho
المصدر: International Journal of Molecular Sciences, Vol 20, Iss 7, p 1593 (2019)
بيانات النشر: MDPI AG, 2019.
سنة النشر: 2019
المجموعة: LCC:Biology (General)
LCC:Chemistry
مصطلحات موضوعية: dehydroabietic acid (DAA), inflammation, NF-κB, AP-1, Biology (General), QH301-705.5, Chemistry, QD1-999
الوصف: Dehydroabietic acid (DAA) is a naturally occurring diterpene resin acid derived from coniferous plants such as Pinus and Picea. Various bioactive effects of DAA have been studied including antibacterial, antifungal, and anticancer activities. However, the anti-inflammatory mechanism of DAA remains unclear. We evaluated the anti-inflammatory effect of DAA in macrophage cell lines. Dehydroabietic acid clearly reduced nitric oxide (NO) production and inflammatory gene expression decreased according to RT-PCR results. Dehydroabietic acid displayed anti-inflammatory activity at the transcriptional level in results from NF-κB- or AP-1-mediated luciferase assays. To identify the DAA target protein, we investigated NF-κB and AP-1 pathways by Western blotting analysis. Dehydroabietic acid suppressed the activity of proto-oncogene tyrosine protein kinase (Src) and spleen tyrosine kinase (Syk) in the NF-κB cascade and transforming growth factor beta-activated kinase 1 (TAK1) in the AP-1 cascade. Using overexpression strategies, we confirmed that DAA targeted these kinases. Our findings demonstrate the anti-inflammatory effects and molecular mechanism of DAA. This suggests that DAA has potential as a drug or supplement to ameliorate inflammation.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1422-0067
Relation: https://www.mdpi.com/1422-0067/20/7/1593; https://doaj.org/toc/1422-0067
DOI: 10.3390/ijms20071593
URL الوصول: https://doaj.org/article/ba5fb29bfc3b4bb291a6d02a44cab86f
رقم الأكسشن: edsdoj.ba5fb29bfc3b4bb291a6d02a44cab86f
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:14220067
DOI:10.3390/ijms20071593