preventionoflipopolysaccharideinducedinjuryby35dicaffeoylquinicacidinendothelialcells
文献类型：期刊论文
| 作者 | Ruopeng ZHA; Wei XU; Wenyi WANG; Li DONG; Yiping WANG
|
| 刊名 | actapharmacologicasinica
 |
| 出版日期 | 2007 |
| 卷号 | 28期号:8页码:1143 |
| 关键词 | 3 Lipopolysaccharide Human dermal microvascular endo-thelial cells Reactive oxygen species Apoptosis Caspase-3 5-dicaffeoylquinic acid |
| ISSN号 | 1671-4083 |
| 英文摘要 | 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-Fe~(2+) 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 μmol/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. |
| 语种 | 英语 |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/288064]  |
| 专题 | 中国科学院上海药物研究所 |
| 作者单位 | 中国科学院上海药物研究所 |
| 推荐引用方式 GB/T 7714 | Ruopeng ZHA,Wei XU,Wenyi WANG,et al. preventionoflipopolysaccharideinducedinjuryby35dicaffeoylquinicacidinendothelialcells[J]. actapharmacologicasinica,2007,28(8):1143. |
| APA | Ruopeng ZHA,Wei XU,Wenyi WANG,Li DONG,&Yiping WANG.(2007).preventionoflipopolysaccharideinducedinjuryby35dicaffeoylquinicacidinendothelialcells.actapharmacologicasinica,28(8),1143. |
| MLA | Ruopeng ZHA,et al."preventionoflipopolysaccharideinducedinjuryby35dicaffeoylquinicacidinendothelialcells".actapharmacologicasinica 28.8(2007):1143. |
入库方式： OAI收割
来源：上海药物研究所
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