Mitoquinone (MitoQ)
目录号 : GC30416
Mitoquinone (MitoQ) 是一种泛醌衍生的抗氧化剂，可以共价连接到亲脂性三苯基膦 (TPP) 阳离子上，专门针对线粒体。
Cas No.:444890-41-9
Sample solution is provided at 25 µL, 10mM.
- Exp Gerontol 189 (2024)：112402.PMID:38484905
- Comp Biochem Phys C (2024)：109942.PMID:38810896
- Sci Rep-Uk 14.1 (2024)：26504.PMID:39489819
- Sci Rep-Uk 14.1 (2024)：26504.PMID:39489819
- Iran J Public Health 53.3 (2024)：614-624.
- Anim Reprod Sci 247 (2022)：107099.PMID:36306716
- Heliyon (2024).
- Nat Rev Mol Cell Bio 13.9 (2024) 653：
Mitoquinone (MitoQ) is a ubiquinone-derived antioxidant that can covalently attach to a lipophilic triphenylphosphonium (TPP) cation, specifically targets mitochondria.[1] MitoQ is usually stored within mitochondria in vivo in order to prevent and protect the cellular damage induced by mitochondrial ROS overproduction and oxidative stress.[2]
In vitro experiment it shown that washed platelets incubated with MitoQ 10 μM (4.8% ± 0.8%) markedly increased calcein-negative population (cytotoxic effect) compared to a non-treated control group; MitoQ 10 μM (8.5% ± 2.2%) induced a significant increase in PS exposure on the platelet membrane when compared to the basal control.[3] In addition, MitoQ (5 μM) inhibited collagen and ADP-induced platelet aggregation in PRP samples. In the meanwhile, MitoQ at 2.5 and 5 μM produced a obvious decrease in ROS production generated by antimycin A or collagen on platelet.[3]
In vivo, treatment with 2.5 mg/kg and 5 mg/kg MitoQ can alleviate mouse lung histologic changes induced by CS (Cigarette smoke).[1] In vivo experiment it shown that mitoquinone treatment with 10 mg/kg/day by gavage after 4 weeks, liver structure obiviously improved in association with a significant decrease in collagen deposition. In the meanwhile, mitoquinone treatment determined a significant reduction in hepatic inflammation and fibrosis. Moreover, TIMP-1, MMP-2, and MMP-13 gene expressions were decreased by Mitoquinone treatment.[4]
References:
[1]. Yang D, et al. Mitoquinone ameliorates cigarette smoke-induced airway inflammation and mucus hypersecretion in mice. Int Immunopharmacol. 2021 Jan;90:107149.
[2]. Chen W, et al. Inhibition of Mitochondrial ROS by MitoQ Alleviates White Matter Injury and Improves Outcomes after Intracerebral Haemorrhage in Mice. Oxid Med Cell Longev. 2020 Jan 4;2020:8285065.
[3]. Méndez D, et al. Mitoquinone (MitoQ) Inhibits Platelet Activation Steps by Reducing ROS Levels. Int J Mol Sci. 2020 Aug 27;21(17):6192.
[4]. Turkseven S, et al. Mitochondria-targeted antioxidant mitoquinone attenuates liver inflammation and fibrosis in cirrhotic rats. Am J Physiol Gastrointest Liver Physiol. 2020 Feb 1;318(2):G298-G304.
Mitoquinone (MitoQ) 是一种泛醌衍生的抗氧化剂，可以共价连接到亲脂性三苯基膦 (TPP) 阳离子上，专门针对线粒体。[1]MitoQ 通常储存在体内线粒体中，以便预防和保护由线粒体 ROS 过量产生和氧化应激引起的细胞损伤。[2]
体外实验表明，与未处理的对照组相比，用 MitoQ 10 μM (4.8% ± 0.8%) 孵育的洗涤过的血小板显着增加了钙黄绿素阴性群体（细胞毒性作用）；与基础对照相比，MitoQ 10 μM (8.5% ± 2.2%) 可显着增加血小板膜上的 PS 暴露。[3] 此外，MitoQ (5 μM) 可抑制胶原蛋白和 ADP -在 PRP 样品中诱导血小板聚集。同时，2.5 和 5 μM 的 MitoQ 显着降低抗霉素 A 或血小板上胶原蛋白产生的 ROS。[3]
在体内，用 2.5 mg/kg 和 5 mg/kg MitoQ 处理可以减轻 CS（香烟烟雾）引起的小鼠肺组织学变化。[1] 体内实验表明，mitoquinone 处理4 周后以 10 mg/kg/天的剂量灌胃，肝脏结构明显改善，胶原蛋白沉积显着减少。同时，线粒体醌治疗可显着减少肝脏炎症和纤维化。此外，丝裂醌处理降低了 TIMP-1、MMP-2 和 MMP-13 基因的表达。[4]
| Cell experiment [1]: | |
|
Cell lines |
Mouse Embryonic Fibroblasts (MEF) |
|
Preparation Method |
Cells were treated with MitoQ for 16 h. Superoxide anion was determined by incubating the cells with 50 nM MitoSox for 30 min. To analyze the effect of MitoQ 0.05 and 0.1 µM on acute oxidative stress, MEFwt cells were incubated with MitoSox in the absence or presence of 5 µM antimycin A. |
|
Reaction Conditions |
0.05 and 0.1 µM, 16h |
|
Applications |
MitoQ at 2.5 and 5 μM produced a significant decrease in ROS production generated by antimycin A or collagen on platelets. |
| Animal experiment [2]: | |
|
Animal model |
Male Sprague-Dawley rats |
|
Preparation Method |
Mitoquinone (10 mg•kg−1•day−1; MitoQ, New Zealand; n = 10) or vehicle (dimethyl sulfoxide 0.7%; n = 10) administration by gavage was started 3 days after CBDL and continued for 4 wk. Three hours after the last administration, rats were euthanized. |
|
Dosage form |
10 mg•kg−1•day−1, p.o. |
|
Applications |
The weight of livers from rats treated with mitoquinone was significantly lower than that of livers from untreated cirrhotic animals and similar to that of controls, likely due to the reduction of hepatic inflammation. |
|
References: |
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| Cas No. | 444890-41-9 | SDF | |
| Canonical SMILES | O=C(C(CCCCCCCCCC[P+](C1=CC=CC=C1)(C2=CC=CC=C2)C3=CC=CC=C3)=C4C)C(OC)=C(OC)C4=O | ||
| 分子式 | C37H44O4P | 分子量 | 583.72 |
| 溶解度 | DMSO : 50 mg/mL (73.66 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。 |
||
| 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 | 1.7132 mL | 8.5658 mL | 17.1315 mL |
| 5 mM | 0.3426 mL | 1.7132 mL | 3.4263 mL |
| 10 mM | 0.1713 mL | 0.8566 mL | 1.7132 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 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % 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。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
-
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The interventions included intravenous administration of saline, Mitoquinone (MitoQ)(GlpBio, USA) at a dosage of 5mg/kg, a combination of GP+EM at a dosage of 5mg/kg GP and 5mg/kg EM, and TK-MLP@(GP+EM) NPs at a dosage of 5mg/kg GP and 5mg/kg EM.
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MitoQ attenuated ERS and ERS-dependent apoptosis by alleviating mitochondrial oxidative damage in HepG2 cells exposed to HFPO-TA. (A) Cell viability of HepG2 cells exposed to 75μM HFPO-TA and/or 5μM MitoQ for 24h. HepG2 cells were pretreated with 5μM MitoQ for 30min.
HepG2 cells were pretreated with 50μM 2-APB and 5μM MitoQ(GlpBio, USA) for 1h and 30min, respectively, followed by exposure to 75μM HFPO-TA for 24h.
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MitoQ attenuated mitochondrial damage and hippocampal injury in AlCl3-treated Parkin-/- mice. (F) Effect of MitoQ on the structure of the hippocampus of mice was observed by observing the microstructure of CA1 and CA3 regions. Yellow arrows indicated degenerated necrotic cells.
The second-time was treated with normal saline, MitoQ(GlpBio, USA)(5mg/kg body weight, twice weekly) or MCC950 (10mg/kg body weight, twice weekly) by intraperitoneal injection in the afternoon of the same day.
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MitoQ alleviated mtROS overproduction, activation of NLRP3-inflammasome and W/β signaling and fibrosis in the T-2 cell model. (L) Cell viability of HK-2 cell.
MitoQ (mtROS scavenger) was given to mice by the intraperitoneal injection28 (GLPBIO, USA, 5mg/kg, twice weekly for 4 weeks).
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(C) DHE staining of mtROS (magnification, 400 × ).
The MitoQ (mtROS scavenger; GLPBIO, USA) was intraperitoneally administered to mice in HFPO-TA + MitoQ group (5 mg/kg, twice/week for 4 weeks).
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