Prevention of lipopolysaccharide-induced injury by 3,5-dicaffeoylquinic acid in endothelial cells
文献类型：期刊论文
| 作者 | Zha, Ruo-peng; Xu, Wei; Wang, Wen-yi; Dong, Li; Wang, Yi-ping
|
| 刊名 | ACTA PHARMACOLOGICA SINICA
 |
| 出版日期 | 2007-08 |
| 卷号 | 28期号:8页码:1143-1148 |
| 关键词 | 3, 5-dicaffeoylquinic acid lipopolysaccharide human dermal microvascular endo-thelial cells reactive oxygen species apoptosis caspase-3 |
| ISSN号 | 1671-4083 |
| DOI | 10.1111/j.1745-7254.2007.00595.x |
| 文献子类 | Article |
| 英文摘要 | Aim: To investigate the effect of 3,5-dicaffeoylquinic acid (3,5-diCQA) on lipopolysaccharide (LPS)-induced injury in human dermal microvascular endothelial cells (HMEC-1). Methods: The anti-oxidant effect was detected using the malondialdehyde (MDA) assay in a rat liver microsome model of lipid peroxidation. Cell viability was analyzed using the 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide assay. Cell lipid peroxide injury was measured by lactate dehydrogenase (LDH) release. Apoptotic cells were detected by flow cytometry, and confirmed by DNA fragmentation analysis. Caspase-3 activity was measured using a specific assay kit. The level of intracellular reactive oxygen species (ROS) was determined by flow cytometry with a 2,7-dichlorodihydrofluorescein diacetate fluorescence probe. Results: The exposure of microsomes to ascorbate-Fe2+ resulted in lipoperoxidation according to an increase in the level of MDA. MDA formation decreased in a dose-dependent manner on treatment with 5, 10, or 50 umol/L 3,5-diCQA. Treatment with LPS for 16 h resulted in a 60% decrease in cell viability and an increase in LDH release from 47.6% to 61.5%. DNA laddering was observed by agarose gel electrophoresis. The level of apoptotic cells peaked at 27% after treatment with LPS for 12 h. Following treatment with LPS for 12 h, intracellular ROS and caspase-3 activity increased. Pre-treatment with 3,5-diCQA at 5, 10, or 50 mu mol/L for 1 h attenuated LPS-mediated endothelial cell injury. The anti-apoptotic action of 3,5-diCQA was partially dependent on its capacity for anti-oxidation and the suppression of caspase-3 activity. Conclusion: 3,5-diCQA displays anti-oxidative and anti-apoptotic activity in HMEC-1 due to scavenging of intracellular ROS induced by LPS, and the suppression of caspase-3 activity. |
| WOS关键词 | NECROSIS-FACTOR-ALPHA ; INDUCED APOPTOSIS ; RAT-LIVER ; LIPID-PEROXIDATION ; NITRIC-OXIDE ; IN-VIVO ; PHENYLETHANOIDS ; ANTIOXIDANTS ; INHIBITION ; EXPRESSION |
| WOS研究方向 | Chemistry ; Pharmacology & Pharmacy |
| 语种 | 英语 |
| CSCD记录号 | CSCD:3088146 |
| WOS记录号 | WOS:000248512000008 |
| 出版者 | BLACKWELL PUBLISHING |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/273181]  |
| 专题 | 药理学第一研究室 中科院受体结构与功能重点实验室 新药研究国家重点实验室 |
| 通讯作者 | Wang, Yi-ping |
| 作者单位 | 1.Chinese Acad Sci, Shanghai Inst Biol Sci, State Key Lab Drug Res, Shanghai Inst Mat Med, Shanghai 201203, Peoples R China 2.Chinese Acad Sci, Grad Sch, Shanghai 201203, Peoples R China |
| 推荐引用方式 GB/T 7714 | Zha, Ruo-peng,Xu, Wei,Wang, Wen-yi,et al. Prevention of lipopolysaccharide-induced injury by 3,5-dicaffeoylquinic acid in endothelial cells[J]. ACTA PHARMACOLOGICA SINICA,2007,28(8):1143-1148. |
| APA | Zha, Ruo-peng,Xu, Wei,Wang, Wen-yi,Dong, Li,&Wang, Yi-ping.(2007).Prevention of lipopolysaccharide-induced injury by 3,5-dicaffeoylquinic acid in endothelial cells.ACTA PHARMACOLOGICA SINICA,28(8),1143-1148. |
| MLA | Zha, Ruo-peng,et al."Prevention of lipopolysaccharide-induced injury by 3,5-dicaffeoylquinic acid in endothelial cells".ACTA PHARMACOLOGICA SINICA 28.8(2007):1143-1148. |
入库方式： OAI收割
来源：上海药物研究所
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