5-Hydroxydecanoate sodium
(Synonyms: 5-羟基癸酸钠盐) 目录号 : GC60029
5-Hydroxydecanoatesodium是一种选择性ATP敏感的K+(KATP)通道阻滞剂(IC50约为30μM)。5-Hydroxydecanoatesodium是线粒体外膜酰基辅酶A合成酶的底物，并具有抗氧化活性。
Cas No.:71186-53-3
Sample solution is provided at 25 µL, 10mM.
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- Purity: >98.00%
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5-Hydroxydecanoate sodium is a selective ATP-sensitive K+ (KATP) channel blocker (IC50 of ~30 μM). 5-Hydroxydecanoate sodium is a substrate for mitochondrial outer membrane acyl-CoA synthetase and has antioxidant activity[1][2].
5-Hydroxydecanoate (5-HD) treatment abolishs the beneficial effects of penehyclidine hydrochloride (PHC) preconditioning in anoxia/reoxygenation (A/R)‐induced injury in H9c2 cells. 5-Hydroxydecanoate blocks the inhibitory effect of PHC on Ca2+ overload and ROS production. 5-Hydroxydecanoate promotes the release of Cyt-C from mitochondria into cytoplasm. 5-Hydroxydecanoate attenuats the anti-apoptotic effect of PHC. PHC treatment shows remarkably decreases levels of Bax and cleaved caspase-3, and increases levels of Bcl-2. 5-Hydroxydecanoate pretreatment reverses the effects of PHC on their expression levels. 5-Hydroxydecanoate blocks the effects of PHC on KATP channels[1].
5-Hydroxydecanoate (100 μM) treatment abolishes the effects of ischemic preconditioning (IPC) on the contractile recovery and does not affect its effect on the contracture, lactate production, glycogenolysis and viable tissue in rats[3].
[1]. Congna Zi, et al. Penehyclidine hydrochloride protects against anoxia/reoxygenation injury in cardiomyocytes through ATP-sensitive potassium channels, and the Akt/GSK-3β and Akt/mTOR signaling pathways. Cell Biol Int. 2020 Jun;44(6):1353-1362. [2]. Xiantao Li, et al. 5-Hydroxydecanoate and coenzyme A are inhibitors of native sarcolemmal KATP channels in inside-out patches. Biochim Biophys Acta. 2010 Mar;1800(3):385-91. [3]. M G Marina Prendes, et al. Effects of 5-hydroxydecanoate and ischemic preconditioning on the ischemic-reperfused heart of fed and fasted rats. J Physiol Biochem. 2005 Sep;61(3):447-56.
| Cas No. | 71186-53-3 | SDF | |
| 别名 | 5-羟基癸酸钠盐 | ||
| Canonical SMILES | CCCCCC(O)CCCC(O[Na])=O | ||
| 分子式 | C10H19NaO3 | 分子量 | 210.25 |
| 溶解度 | DMSO : 12.5 mg/mL (59.45 mM; Need ultrasonic); H2O : 10 mg/mL (47.56 mM; Need ultrasonic) | 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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1 mg | 5 mg | 10 mg |
| 1 mM | 4.7562 mL | 23.7812 mL | 47.5624 mL |
| 5 mM | 0.9512 mL | 4.7562 mL | 9.5125 mL |
| 10 mM | 0.4756 mL | 2.3781 mL | 4.7562 mL |
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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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2.
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Diazoxide decreases ischemia-reperfusion injury in a rat model of lung transplantation
Transplant Proc 2011 Sep;43(7):2510-6.PMID:21911115DOI:10.1016/j.transproceed.2011.04.015.
Background: Ischemia-reperfusion injury (IRI) is a significant factor contributing to primary graft failure in lung transplantation. Given a pivotal role of mitochondria in IRI-related molecular events, the effects of diazoxide, a selective opener of mitochondrial adenosine-5'-triphosphate (ATP)-sensitive potassium channels (mitoK(ATP)), on IRI were investigated in a rat model of lung transplantation. Methods: The 108 rats were randomly assigned to 5 groups; a sham-operated, 2 control, and 2 experimental groups that received either diazoxide alone or a combination of diazoxide with 5-Hydroxydecanoate sodium salt. Lung injuries were assessed by multiple parameters at 2 hours or 24 hours after reperfusion, including oxygenation index, wet/dry weight ratio of transplanted lungs, lung morphology, as well as measurements of myeloperoxidase, malondialdehyde, total antioxidant capacity, tumor necrosis factor-α, and interleukin-6. Results: Compared with the sham group, the 2 control groups revealed significant changes among most parameters of lung injury measured at either 2 hours or 24 hours after reperfusion. The extent of the changes was dramatically reduced by the administration of diazoxide. Importantly, the protective effect of diazoxide was almost completely reversed by co-administration of 5-Hydroxydecanoate sodium salt, a selective blocker of mitoK(ATP). Conclusions: These data provide evidence for substantial protective effects of diazoxide in an in vivo rat lung IRI model. Pharmacological modulation of mitoK(ATP) may be a potential strategy to reduce IRI-induced primary graft failure in lung transplantation.
Hydrogen gas post-conditioning attenuates early neuronal pyroptosis in a rat model of subarachnoid hemorrhage through the mitoKATP signaling pathway
Exp Ther Med 2021 Aug;22(2):836.PMID:34149882DOI:10.3892/etm.2021.10268.
Neuronal pyroptosis serves an important role in the progress of neurologic dysfunction following subarachnoid hemorrhage (SAH), which is predominantly caused by a ruptured aneurysm. Hydrogen gas has been previously reported to be an effective anti-inflammatory agent against ischemia-associated diseases by regulating mitochondrial function. The objective of the present study was to investigate the potential neuroprotective effects of hydrogen gas post-conditioning against neuronal pyroptosis after SAH, with specific focus on the mitochondrial ATP-sensitive K+ (mitoKATP) channels. Following SAH induction by endovascular perforation, rats were treated with inhalation of 2.9% hydrogen gas for 2 h post-perforation. Neurologic deficits, brain water content, reactive oxygen species (ROS) levels, neuronal pyroptosis, phosphorylation of ERK1/2, p38 MAPK and pyroptosis-associated proteins IL-1β and IL-18 were evaluated 24 h after perforation by a modified Garcia method, ratio of wet/dry weight, 2',7'-dichlorofluorescin diacetate, immunofluorescence and western blot assays, respectively. An inhibitor of the mitoKATP channel, 5-Hydroxydecanoate sodium (5-HD), was used to assess the potential role of the mitoKATP-ERK1/2-p38 MAPK signal pathway. Hydrogen gas post-conditioning significantly alleviated brain edema and improved neurologic function, reduced ROS production and neuronal pyroptosis, suppressed the expression of IL-1β and IL-18 whilst upregulating ERK1/2 phosphorylation, but downregulated p38 MAPK activation 24 h post-SAH. These aforementioned effects neuroprotective were partially reversed by 5-HD treatment. Therefore, these observations suggest that post-conditioning with hydrogen gas ameliorated SAH-induced neuronal pyroptosis at least in part through the mitoKATP/ERK1/2/p38 MAPK signaling pathway.