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- 保存条件：
Powder:2-8℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year
- 保质期：
Powder:2-8℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year
- 英文名：
Auranofin
- 库存：
现询
- 供应商：
北京索莱宝科技有限公司
- CAS号：
34031-32-8
- 规格：
50mg
【本资料源自公开渠道，如需（此处）屏蔽，请联系删除】
标题:Glyoxal damages human aortic endothelial cells by perturbing the glutathione, mitochondrial membrane potential, and mitogen-activated protein kinase pathways
成员:Xie Ming-Zhang, Guo Chun, Dong Jia-Qi, Zhang Jie, Sun Ke-Tao, Lu Guang-Jian, Wang Lei, Bo De-Ying, Jiao Lu-Yang, Zhao Guo-An
论文因子:2.298 发表期刊:BMC Cardiovascular Disorders pmid:34922451
【本资料源自公开渠道，如需（此处）屏蔽，请联系删除】
标题:Glyoxal damages human aortic endothelial cells by perturbing the glutathione; mitochondrial membrane potential; and mitogen-activated protein kinase pathways
成员:Xie MZ， Guo C， Dong JQ， Zhang J， Sun KT， Lu GJ， Wang L， Bo DY， Jiao LY， Zhao GA.
论文因子:2.1 发表期刊:BMC Cardiovascular Disorders pmid:34922451
【本资料源自公开渠道，如需（此处）屏蔽，请联系删除】
标题:Glyoxal damages human aortic endothelial cells by perturbing the glutathione; mitochondrial membrane potential; and mitogen-activated protein kinase pathways
成员:Xie MZ; Guo C; Dong JQ; Zhang J; Sun KT; Lu GJ; Wang L; Bo DY; Jiao LY; Zhao GA.
论文因子:2.1 发表期刊:BMC Cardiovascular Disorders pmid:34922451
| 基本信息 | |
| CAS | No.34031-32-8 |
| 中文名称 | 金诺芬 |
| 英文名称 | Auranofin |
| 别名 | 醋硫葡金;SKF-39162 |
| 分子式 | C₂₀H₃₄AuO₉PS |
| 分子量 | 678.49 |
| 溶解性 | Soluble in DMSO ≥5mg/mL(Need ultrasonic) |
| 纯度 | ≥98% |
| 外观(性状) | White to off-white Solid |
| 储存条件 | Powder:2-8℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year |
| MDL | MFCD00080759 |
| SMILES | CCP(CC)CC.CC(=O)OCC1C(C(C(C(O1)[S-])OC(=O)C)OC(=O)C)OC(=O)C.[Au+] |
| InChIKey | AUJRCFUBUPVWSZ-UHFFFAOYSA-M |
| InChI | InChI=1S/C14H20O9S.C6H15P.Au/c1-6(15)19-5-10-11(20-7(2)16)12(21-8(3)17)13(14(24)23-10)22-9(4)18;1-4-7(5-2)6-3;/h10-14，24H，5H2，1-4H3;4-6H2，1-3H3;/q;;+1/p-1 |
| PubChem CID | 24199313 |
| 靶点 | thioredoxin reductase (TrxR) |
| 通路 | Metabolic Enzyme&Protease |
| 背景说明 | Auranofin是硫氧还蛋白还原酶 (TrxR) 的抑制剂。 |
| 生物活性 | Auranofin (SKF-39162) is a thioredoxin reductase (TrxR) inhibitor with an IC50 of 0.2 μM. Auranofin exhibits antiviral activity against SARS-CoV21， with a CC50 of 4.2?μM for monkey kidney Vero E6 cells.[1-5] |
| IC50 | IC50: 0.2 μM (TrxR)[1] |
| In Vitro | Treatment with auranofin significantly inhibited cell viability with an IC50 value of 2.5 μM after 24 h. In particular， when cells were treated with 2.5 μM auranofin， there was a 2.2-fold increase in apoptotic cells compared to untreated cells. Auranofin activated Caspase-3 and -8 in a concentration-dependent manner and decreased the levels of mitochondrial anti-apoptotic factors， such as Bcl-2 and Bcl-xL.[3]。 |
| 细胞实验 | Adjuvant - induced arthritis (AA) in rats is associated with a number of immunologic abnormalities which include a marked decrease in spleen cell mitogenic responses.In this study we investigated the altered production of interleukins in arthritic rats and evaluated the effects of auranofin treatment on disease progression and aberrant interleukin production.The capacity of the AA rat spleen cells to produce interleukin (IL) 2 and IL - 3 was found to decrease during the development of the arthritic lesion， with maximum suppression occurring 16 to 17 days after adjuvant injection. In contrast， the production of IL - 1 by splenic adherent cells from arthritic rats was markedly increased.Prophylactic treatment of AA rats with auranofin resulted in a slight reduction in paw edema， a complete normalization of the depressed IL - 2 production， and a reduction of the elevated IL - 1 production， but had no effect on the depressed IL - 3 production.In contrast， auranofin administered to normal rats， in the same dosing regimen， did not affect interleukin production.Therapeutic administration of auranofin to AA rats with established disease resulted in normalization of IL - 1 production without affecting the suppressed IL - 2 and IL - 3 levels.In contrast， while indomethacin treatment effectively decreased paw edema， it did not appreciably affect the systemic aberrant interleukin production.[4]。 |
| 细胞实验 | Auranofin is dissolved in DMSO. Cells are treated with auranofin (0， 50， 100， 200 and 400 nM) for 72 h for the dose-dependent response assay and 100 nM of auranofin is added into the wells for 0， 24， 72 and 120 h for the time-dependent response assay. Control cultures are treated with DMSO. Cell viability is measured by the MTT assay[2]. |
| 动物实验 | Rats: Prophylactically， auranofin (6.7 to 15 mg of gold/kg)， indomethacin (2 mg/kg) or tragacanth vehicle control were administered orally at daily intervals beginning on the day of adjuvant injection. On days 16 to 17 peritoneal exudate cells or spleen cells from normal or adjuvant-injected rats were isolated and tested[4]. |
| 数据来源文献 | [1]. Cox AG， et al. The thioredoxin reductase inhibitor auranofin triggers apoptosis through a Bax/Bak-dependent process that involves peroxiredoxin 3 oxidation. Biochem Pharmacol. 2008 Oct 30;76(9):1097-109. [2]. Park SH， et al. Auranofin displays anticancer activity against ovarian cancer cells through FOXO3 activation independent of p53. Int J Oncol. 2014 Oct;45(4):1691-8. [3]. Park N， et al. Auranofin promotes mitochondrial apoptosis by inducing annexin A5 expression and translocation in human prostate cancer cells. J Toxicol Environ Health A. 2014;77(22-24):1467-76. [4]. Lee JC， et al. Effect of auranofin treatment on aberrant splenic interleukin production in adjuvant arthritic rats. J Immunol. 1987 Nov 15;139(10):3268-74. [5]. Shuofeng Yuan， et al. Metallodrug ranitidine bismuth citrate suppresses SARS-CoV-2 replication and relieves virus-associated pneumonia in Syrian hamsters. Nat Microbiol. 2020 Oct 7. |
| 单位 | 瓶 |
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文献和实验【本资料源自公开渠道，如需（此处）屏蔽，请联系删除】
标题:Glyoxal damages human aortic endothelial cells by perturbing the glutathione, mitochondrial membrane potential, and mitogen-activated protein kinase pathways
成员:Xie Ming-Zhang, Guo Chun, Dong Jia-Qi, Zhang Jie, Sun Ke-Tao, Lu Guang-Jian, Wang Lei, Bo De-Ying, Jiao Lu-Yang, Zhao Guo-An
论文因子:2.298 发表期刊:BMC Cardiovascular Disorders pmid:34922451
【本资料源自公开渠道，如需（此处）屏蔽，请联系删除】
标题:Glyoxal damages human aortic endothelial cells by perturbing the glutathione; mitochondrial membrane potential; and mitogen-activated protein kinase pathways
成员:Xie MZ， Guo C， Dong JQ， Zhang J， Sun KT， Lu GJ， Wang L， Bo DY， Jiao LY， Zhao GA.
论文因子:2.1 发表期刊:BMC Cardiovascular Disorders pmid:34922451
【本资料源自公开渠道，如需（此处）屏蔽，请联系删除】
标题:Glyoxal damages human aortic endothelial cells by perturbing the glutathione; mitochondrial membrane potential; and mitogen-activated protein kinase pathways
成员:Xie MZ; Guo C; Dong JQ; Zhang J; Sun KT; Lu GJ; Wang L; Bo DY; Jiao LY; Zhao GA.
论文因子:2.1 发表期刊:BMC Cardiovascular Disorders pmid:34922451
磷酰胺（DEPC) (Sigma) 、30% 甘油及蛋白酶抑制剂 [ 含有 1 μg/ml 抑肽酶（aprotinin) 、1 μg/ml 胃蛋白酶抑制剂（pepstatin) 、1 μg/ml 亮抑酶肽（leupeptin) 、0.1 mmol/L PMSF ] ，所有药品都来自于 Sigma ( 见注释 1 和注释 2) 。注意：媒介中的两种成分—— DEPC 和 β-巯基乙醇是有毒的，需要在通风橱中进行准备，并需要戴化学防护手套。 2.2 细胞核的提纯 ( 1 ) 样品
to barley yellow dwarf virus. Y i C h u a n 29, 97-102. 36. Y a n , F . , Z h en g , Y. Y. , Z h a n g s W. W . , X ia o , H . , L i, S. F . a n d C h en g s Z . M . (2006) O b ta in ed transgeic w h ea t exp ressin
。它包括APC摄取抗原加工成多肽分子，MHCⅠ或MHCⅡ灯分子将抗原信息分别呈递给CD8或CD4细胞，激活特异性T细胞反应等一系列过程。该过程又分为MHCⅠ和MHCⅡ类分子限制性抗原呈递两条途径[4]。 1.MHCⅠ类分子限制性抗原呈递：MHCⅠ类分子限制的抗原加工和呈递是与胞生物合成MHCⅠ分子的转运相关联的。多数有核细胞都转录并表达MHCⅠ类基因，并预定方式将MHCⅠ类分子的重链和轻链（β2微球蛋白）转运入内质网腔。内源性和外源性蛋白经细胞质中蛋白酶降解形成的短多肽，被位于内质
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