Salidroside Inhibits Endogenous Hydrogen Peroxide Induced Cytotoxicity of Endothelial Cells
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- Zhao Xingyu
- Jilin Medical College
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- Jin Lianhai
- Jilin Medical College
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- Shen Nan
- Jilin Medical College
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- Xu Bin
- Jilin Medical College
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- Zhang Wei
- Jilin Medical College
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- Zhu Hongli
- College of Life Science, Northwest University National Engineering Research Center for Miniaturized Detection Systems, Northwest University
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- Luo Zhengli
- Jilin Medical College
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抄録
Salidroside, a phenylpropanoid glycoside isolated from Rhodiola rosea L., shows potent antioxidant property. Herein, we investigated the protective effects of salidroside against hydrogen peroxide (H2O2)-induced oxidative damage in human endothelial cells (EVC-304). EVC-304 cells were incubated in the presence or absence of low steady states of H2O2 (3–4 µM) generated by glucose oxidase (GOX) with or without salidroside. 3(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione (GSH) assays were performed, together with Hoechst 33258 staining and flow cytometric analysis using Annexin-V and propidium iodide (PI) label. The results indicated that salidroside pretreatment attenuated endogenous H2O2 induced apoptotic cell death in EVC-304 cells in a dose-dependent pattern. Furthermore, Western blot data revealed that salidroside inhibited activation of caspase-3, 9 and cleavage of poly(ADP-ribose) polymerase (PARP) induced by endogenous H2O2. It also decreased the expression of Bax and rescued the balance of pro- and anti-apoptotic proteins. All these results demonstrated that salidroside may present a potential therapy for oxidative stress in cardiovascular and cerebrovascular diseases.
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 36 (11), 1773-1778, 2013
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390001204633013888
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- NII論文ID
- 130003361549
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- NII書誌ID
- AA10885497
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- COI
- 1:STN:280:DC%2BC3sbhvVCruw%3D%3D
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 024957767
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- PubMed
- 23965749
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可