Mito-TEMPO
目录号 : GC31682Mito-Tempo 是一种靶向线粒体的抗氧化剂,具有有效的超氧化物清除特性,可将有毒的超氧化物分子转化为过氧化氢或氧气,随后通过过氧化氢酶或谷胱甘肽过氧化物酶解毒为氧气和水 .在体外,Mito-Tempo 通过增强超氧化物歧化酶 (SOD) 活性和 PI3K/AKT/mTOR 磷酸化而具有更强的保护作用。
Cas No.:1334850-99-5
Sample solution is provided at 25 µL, 10mM.
Mito-Tempo is a mitochondria-targeted antioxidant with effective superoxide scavenging properties, which converts toxic superoxide molecules into hydrogen peroxide or oxygen and subsequently detoxified to oxygen and water by catalase or glutathione peroxidase[1].
In vitro, Mito-Tempo has a greater protective effect by enhancing superoxide dismutase (SOD) activity and PI3K/AKT/mTOR phosphorylation. Glutamate-exposed cells significantly increased cellular oxidative stress by enhancing ROS production. Glutamate treatment also increased LDH release follows the loss of mitochondrial membrane potential, caused cell viability loss. Treatment with Mito-Tempo not only attenuated the generation of ROS and improved mitochondrial membrane potential but also reduced the neurotoxicity of glutamate in a concentration-dependent manner, which leads to increased cell viability and decreased LDH release[2]
In vivo,Mito-TEMPO pretreatment inhibited inflammation, attenuated LPS-induced liver injury, and enhanced the antioxidative capability in septic mice, as evidenced by the decreased MDA content and the increased SOD activity. In addition, Mito-TEMPO restored mitochondrial size and improved mitochondrial function. Finally, we found that the levels of pyroptosis-related proteins in the liver of LPS-treated mice were lower after pretreatment with Mito-TEMPO [3]
References:
[1]. Liang HL, Sedlic F, et al. SOD1 and MitoTEMPO partially prevent mitochondrial permeability transition pore opening, necrosis, and mitochondrial apoptosis after ATP depletion recovery. Free Radic Biol Med. 2010 Nov 30;49(10):1550-60.
[2]. Mukem S, Thongbuakaew T, et al. Mito-Tempo suppresses autophagic flux via the PI3K/Akt/mTOR signaling pathway in neuroblastoma SH-SY5Y cells. Heliyon. 2021 Jun 15;7(6):e07310.
[3]. Mukem S, Thongbuakaew T, et al. Mito-Tempo suppresses autophagic flux via the PI3K/Akt/mTOR signaling pathway in neuroblastoma SH-SY5Y cells. Heliyon. 2021 Jun 15;7(6):e07310.
Mito-Tempo 是一种靶向线粒体的抗氧化剂,具有有效的超氧化物清除特性,可将有毒的超氧化物分子转化为过氧化氢或氧气,随后通过过氧化氢酶或谷胱甘肽过氧化物酶解毒为氧气和水[1] .
在体外,Mito-Tempo 通过增强超氧化物歧化酶 (SOD) 活性和 PI3K/AKT/mTOR 磷酸化而具有更强的保护作用。暴露于谷氨酸的细胞通过增强 ROS 的产生显着增加细胞氧化应激。谷氨酸处理还增加了线粒体膜电位丧失后 LDH 的释放,导致细胞活力丧失。 Mito-Tempo 处理不仅减少了 ROS 的产生并改善了线粒体膜电位,而且以浓度依赖性方式降低了谷氨酸的神经毒性,从而导致细胞活力增加和 LDH 释放减少[2]
在体内,Mito-TEMPO 预处理可抑制炎症,减轻 LPS 诱导的肝损伤,并增强脓毒症小鼠的抗氧化能力,这可以通过降低 MDA 含量和增加 SOD 活性来证明。此外,Mito-TEMPO 恢复了线粒体大小并改善了线粒体功能。最后,我们发现在用 Mito-TEMPO [3]
预处理后,LPS 处理的小鼠肝脏中焦亡相关蛋白的水平较低
Cell experiment [1]: | |
Cell lines |
Human neuroblastoma cells (SH-SY5Y ) |
Preparation Method |
SH-SY5Y cells were treated with 100 μM glutamate in the presence or absence of Mito-Tempo for 24 h. The cell viability was assessed by the mitochondrial performance, using the MTT reduction assay. |
Reaction Conditions |
50, 100 µM Mito-Tempo for 24h. |
Applications |
10 and 100 μM glutamate significantly reduced the number of the living cell to 88.86 ± 3.45% and 51.12 ± 2.97%. 50 and 100 μM Mito-Tempo significantly restored cell viability to 82.90 ± 1.78% and 93.56 ± 2.85%, respectively, indicating that Mito-Tempo could protect the cells from glutamate toxicity. |
Animal experiment [2]: | |
Animal models |
C57BL/6 mice |
Preparation Method |
Lipopolysaccharide- (LPS-) induced experimental sepsis mouse model was established by injecting male mice intraperitoneally with LPS. Mito-TEMPO was intraperitoneally injected 1 h prior to LPS injection. |
Dosage form |
20 mg/kg Mito-TEMPO, intraperitoneal(i.p.) injection |
Applications |
In the LPS+Mito-TEMPO group, the levels of alanine transaminase(ALT) and aspartate transaminase (AST) were approximately 1.5- and 2-fold lower compared with those in the LPS group. Mito-TEMPO pretreatment protects mice against LPS-Induced acute liver injury. |
References: [1]. Mukem S, Thongbuakaew T, et al. Mito-Tempo suppresses autophagic flux via the PI3K/Akt/mTOR signaling pathway in neuroblastoma SH-SY5Y cells. Heliyon. 2021 Jun 15;7(6):e07310. [2]. Wang PF, Xie K, et al. Hepatoprotective Effect of Mitochondria-Targeted Antioxidant Mito-TEMPO against Lipopolysaccharide-Induced Liver Injury in Mouse. Mediators Inflamm. 2022 Jun 20;2022:6394199. |
Cas No. | 1334850-99-5 | SDF | |
Canonical SMILES | [O]N1C(C)(C)CC(NC(C[P+](C2=CC=CC=C2)(C3=CC=CC=C3)C4=CC=CC=C4)=O)CC1(C)C.[Cl-] | ||
分子式 | C29H35ClN2O2P | 分子量 | 510.03 |
溶解度 | DMSO : 125 mg/mL (245.08 mM) | 储存条件 | Store at -20°C |
General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效。 储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。 为了提高溶解度,请将管子加热至37℃,然后在超声波浴中震荡一段时间。 |
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Shipping Condition | 评估样品解决方案:配备蓝冰进行发货。所有其他可用尺寸:配备RT,或根据请求配备蓝冰。 |
制备储备液 | |||
1 mg | 5 mg | 10 mg | |
1 mM | 1.9607 mL | 9.8033 mL | 19.6067 mL |
5 mM | 0.3921 mL | 1.9607 mL | 3.9213 mL |
10 mM | 0.1961 mL | 0.9803 mL | 1.9607 mL |
第一步:请输入基本实验信息(考虑到实验过程中的损耗,建议多配一只动物的药量) | ||||||||||
给药剂量 | mg/kg | 动物平均体重 | g | 每只动物给药体积 | ul | 动物数量 | 只 | |||
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% DMSO % % Tween 80 % saline | ||||||||||
计算重置 |
计算结果:
工作液浓度: mg/ml;
DMSO母液配制方法: mg 药物溶于 μL DMSO溶液(母液浓度 mg/mL,
体内配方配制方法:取 μL DMSO母液,加入 μL PEG300,混匀澄清后加入μL Tween 80,混匀澄清后加入 μL saline,混匀澄清。
1. 首先保证母液是澄清的;
2.
一定要按照顺序依次将溶剂加入,进行下一步操作之前必须保证上一步操作得到的是澄清的溶液,可采用涡旋、超声或水浴加热等物理方法助溶。
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Quality Control & SDS
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- Purity: >98.00%
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