EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #100-0572_C
维生素E类似物
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总览
Trolox是一种细胞渗透性、亲水的维生素E类似物（Choe et al.；Lee et al.）。在小鼠中，Trolox已被证明通过下调NF-κB受体活化因子配体（RANKL）诱导和c-Fos表达来抑制破骨细胞形成（Lee et al.）。Trolox还能阻止顺铂诱导的肾上皮细胞凋亡（Xiao et al.）。
分化
·诱导人胚胎干细胞向β样细胞分化（Petersen et al.）。
癌症研究
·增强骨髓瘤和乳腺癌细胞中砷介导的细胞凋亡（Diaz et al.）。
别名
6-羟基-2,5,7,8-四甲基色烷-2-羧酸
细胞类型
癌细胞及细胞系，胰腺细胞
应用
分化
研究领域
癌症，干细胞生物学
CAS 编号
53188-07-1
化学式
C14H18O4
分子量
250.3 g/mol
纯度
≥98%
通路
WNT
产品说明书及文档
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相关材料与文献
技术资料 (4)
文献 (5)
Possible involvement of oxidative stress in cisplatin-induced apoptosis in LLC-PK1 cells.
Journal of toxicology and environmental health. Part A 2003 mar
Abstract
Use of cisplatin,a chemotherapeutic agent,is associated with toxicity as a significant number of patients develop a decline in renal function. The mechanisms by which cisplatin produces renal injury are not well understood. It has been suggested that free radical-catalyzed lipid peroxidation can induce apoptosis or necrosis leading to renal injury. This study examined whether low concentrations of cisplatin induce apoptosis in LLC-PK1 cells and whether caspases 1,2,3,8,and 9 are activated during this event. Our results show a dose- and time-dependent induction of apoptosis by micromolar concentrations of cisplatin. Expression of oncogenes c-myc and p53 was induced,and except for caspase 1,all the other caspases tested were activated. Z-VAD,the broad-spectrum inhibitor of caspases,prevented caspase activation and apoptosis,but not c-myc and p53 induction. On the other hand,N-acetylcysteine prevented cisplatin-induced apoptosis as well as c-myc induction but not p53 induction. The antioxidant trolox also prevented cisplatin-induced apoptosis. The results suggest that antioxidants and caspase inhibitors may alleviate cisplatin-associated nephrotoxicity.
Trolox selectively enhances arsenic-mediated oxidative stress and apoptosis in APL and other malignant cell lines.
Blood 2005 feb
Abstract
Although arsenic trioxide (As(2)O(3)) is an effective therapy in acute promyelocytic leukemia (APL),its use in other malignancies is limited by the toxicity of concentrations required to induce apoptosis in non-APL tumor cells. We looked for agents that would synergize with As(2)O(3) to induce apoptosis in malignant cells,but not in normal cells. We found that trolox (6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid),a widely known antioxidant,enhances As(2)O(3)-mediated apoptosis in APL,myeloma,and breast cancer cells. Treatment with As(2)O(3) and trolox increased intracellular oxidative stress,as evidenced by heme oxygenase-1 (HO-1) protein levels,c-Jun terminal kinase (JNK) activation,and protein and lipid oxidation. The synergistic effects of trolox may be specific to As(2)O(3),as trolox does not add to toxicity induced by other chemotherapeutic drugs. We explored the mechanism of this synergy using electron paramagnetic resonance and observed the formation of trolox radicals when trolox was combined with As(2)O(3),but not with doxorubicin. Importantly,trolox protected nonmalignant cells from As(2)O(3)-mediated cytotoxicity. Our data provide the first evidence that trolox may extend the therapeutic spectrum of As(2)O(3). Furthermore,the combination of As(2)O(3) and trolox shows potential specificity for tumor cells,suggesting it may not increase the toxicity associated with As(2)O(3) monotherapy in vivo.
Trolox prevents osteoclastogenesis by suppressing RANKL expression and signaling.
The Journal of biological chemistry 2009 may
Abstract
Excessive receptor activator of NF-kappaB ligand (RANKL) signaling causes enhanced osteoclast formation and bone resorption. Thus,down-regulation of RANKL expression or its downstream signals may be a therapeutic approach to the treatment of pathological bone loss. In this study,we investigated the effects of Trolox,a water-soluble vitamin E analogue,on osteoclastogenesis and RANKL signaling. Trolox potently inhibited interleukin-1-induced osteoclast formation in bone marrow cell-osteoblast coculture by abrogating RANKL induction in osteoblasts. This RANKL reduction was attributed to the reduced production of prostaglandin E(2) via a down-regulation of cyclooxygenase-2 activity. We also found that Trolox inhibited osteoclast formation from bone marrow macrophages induced by macrophage colony-stimulating factor plus RANKL in a reversible manner. Trolox was effective only when present during the early stage of culture,which implies that it targets early osteoclast precursors. Pretreatment with Trolox did not affect RANKL-induced early signaling pathways,including MAPKs,NF-kappaB,and Akt. We found that Trolox down-regulated the induction by RANKL of c-Fos protein by suppressing its translation. Ectopic overexpression of c-Fos rescued the inhibition of osteoclastogenesis by Trolox in bone marrow macrophages. Trolox also suppressed interleukin-1-induced osteoclast formation and bone loss in mouse calvarial bone. Taken together,our findings indicate that Trolox prevents osteoclast formation and bone loss by inhibiting both RANKL induction in osteoblasts and c-Fos expression in osteoclast precursors.
更多信息
| Molecular Weight | 250.3 g/mol |
|---|---|
| Alternative Names | 6-Hydroxy-2, 5, 7, 8-tetramethylchroman-2-carboxylic acid |
| Cas Number | 53188-07-1 |
| Chemical Formula | C14H18O4 |
| 纯度 | ≥ 98% |
| Pathway | WNT |
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