دورية أكاديمية

Inhibition of PDGF-BB-induced proliferation and migration in VSMCs by proanthocyanidin A2: Involvement of KDR and Jak-2/STAT-3/cPLA2 signaling pathways.

التفاصيل البيبلوغرافية
العنوان: Inhibition of PDGF-BB-induced proliferation and migration in VSMCs by proanthocyanidin A2: Involvement of KDR and Jak-2/STAT-3/cPLA2 signaling pathways.
المؤلفون: Zhang, Liudi1, Shao, Jie2, Zhou, Yufu1, Chen, Haifei1, Qi, Huijie1, Wang, Yi1, Chen, Lu1, Zhu, Yongjun3 zhuyongjun@huashan.org.cn, Zhang, Meng4, Chen, Li5, Du, Yongli6, Zhong, Mingkang1, Shi, Xiaojin1, Li, Qunyi1 qyli1234@163.com
المصدر: Biomedicine & Pharmacotherapy. Feb2018, Vol. 98, p847-855. 9p.
مصطلحات موضوعية: *PROANTHOCYANIDINS, *CELL proliferation, *CELL migration, *JAK-STAT pathway, *ANTIOXIDANTS, *ANTI-inflammatory agents
مستخلص: Proanthocyanidin A2 (PA2), one of A-type proanthocyanidins, has been shown to harbor a broad spectrum of pharmacological activities, including anti-inflammatory, antioxidant, anti-HIV, anti-CDV and anti-α-glucosidase activities. However, little is known about the role for PA2 in regulating PDGF-induced VSMC proliferation and migration. In the present study, we investigated the possible effects of PA2 on PDGF-BB-induced proliferation, migration and inflammation in VSMCs in vitro to mimic a postangioplasty PDGF shedding condition. Herein, the data clearly show that PA2 markedly inhibited proliferation, migration and inflammatory responses at 0–30 μg/ml concentration in VSMCs in vitro . 10–30 μg/ml PA2 inhibited PDGF-mediated NAD(P)H oxidase activation and intracellular ROS formation in VSMCs. Furthermore, the effects exerted by PA2 involve the participation of KDR and Jak-2/STAT-3/cPLA 2 signaling pathways. These data also highlight the possible therapeutic use of PA2 in vascular proliferative diseases, where abnormal proliferation and migration play important pathological roles. [ABSTRACT FROM AUTHOR]
قاعدة البيانات: Academic Search Index
الوصف
تدمد:07533322
DOI:10.1016/j.biopha.2018.01.010