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学科主题: 药学
题名:
Hydroxysafflor yellow A enhances survival of vascular endothelial cells under hypoxia via upregulation of the HIF-1 alpha-VEGF pathway and regulation of Bcl-2/Bax
作者: Ji, Deng Bo1,2,3; Zhu, Mei Cai4; Zhu, Bing5,6; Zhu, Yi Zhun7,8,9; Li, Chang Ling1; Ye, Jia1; Zhu, Hai Bo2,3
关键词: hydroxysafflor yellow A ; endothelial cell ; apoptosis ; VEGF ; HIF-1 alpha ; Bcl-2/Bax
刊名: JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
发表日期: 2008-08-01
卷: 52, 期:2, 页:191-202
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Cardiac & Cardiovascular Systems ; Pharmacology & Pharmacy
研究领域[WOS]: Cardiovascular System & Cardiology ; Pharmacology & Pharmacy
关键词[WOS]: EMBRYONIC STEM-CELLS ; GROWTH-FACTOR ; INDUCED APOPTOSIS ; OXIDATIVE STRESS ; IN-VITRO ; ANGIOGENESIS ; EXPRESSION ; MECHANISMS ; PROTEINS ; VESSELS
英文摘要:

Hydroxysafflor yellow A (HSYA) is a component of the flower Carthamus tinctorius L. The present investigation determines whether HSYA can modify the effects of hypoxia on vascular endothelial cells (EC) and its mechanisms. Human EC line (EAhy926) viability was determined using the MTT assay. EC cycle phase distribution was done with PI staining and flow cytometric analysis, and EC apopotsis was done AnnexinV-FITC detection and the TUNEL assay. The protein levels of VEGF, Bcl-2, Bax, and HIF-1 alpha were determined by ELISA or western blot analysis, and the mRNA expression of these genes by RT-PCR analysis. HIF-1 alpha transcriptional activity was measured using a reporter gene assay. HSYA improved cell viability under hypoxia in a concentration-dependent manner by attenuating its cycle arrest and inhibiting its apoptosis. HSYA upregulated the bcl-2/bax ratio, which is down-regulated under hypoxia, increased VEGF protein accumulation and its transcriptional activity. In conclusion, HSAY could enhance the survival of ECs under hypoxia, which may be correlated with its effect of upregulating the bcl-2/bax ratio and promoting HIF-1 alpha protein accumulation, which increases VEGF. These findings provide evidence for the mechanisms by which HSYA maintains EC survival under hypoxia.

语种: 英语
所属项目编号: 30370720 ; 30572343 ; 2004CB518906 ; IRT0514
项目资助者: National Natural Sciences Foundation of China (NSFC) ; National 973 Fundamental Project of China ; Program for Changiiang Scholars and Innovative Research Team in University (PCSIRT)
WOS记录号: WOS:000258798000011
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/64780
Appears in Collections:北京大学药学院_期刊论文

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作者单位: 1.Peking Univ, Sch Pharmaceut Sci, Dept Mol & Cellular Pharmacol, Beijing 100191, Peoples R China
2.Chinese Acad Med Sci, Inst Mat Med, Minist Educ, Key Lab Bioact Substances & Resources Utilizat Ch, Beijing 100050, Peoples R China
3.Peking Union Med Coll, Beijing 100021, Peoples R China
4.Gen Hosp AF Peoples Liberat China, Dept Mol Biol, Beijing, Peoples R China
5.Univ S Alabama, Coll Med, Dept Pharmacol, Mobile, AL 36688 USA
6.Univ S Alabama, Coll Med, Ctr Lung Biol, Mobile, AL USA
7.Fudan Univ, Inst Biomed Sci, Shanghai 200433, Peoples R China
8.Natl Univ Singapore, Fac Med, Dept Pharmacol, Singapore 117548, Singapore
9.Fudan Univ, Dept Pharmacol, Sch Pharm, Shanghai 200433, Peoples R China

Recommended Citation:
Ji, Deng Bo,Zhu, Mei Cai,Zhu, Bing,et al. Hydroxysafflor yellow A enhances survival of vascular endothelial cells under hypoxia via upregulation of the HIF-1 alpha-VEGF pathway and regulation of Bcl-2/Bax[J]. JOURNAL OF CARDIOVASCULAR PHARMACOLOGY,2008,52(2):191-202.
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