H135
5-羟基癸酸 钠盐
≥97% (HPLC)
别名:
5-羟基癸酸 钠盐
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关于此项目
经验公式（希尔记法）:
C10H19NaO3
化学文摘社编号:
分子量:
210.25
NACRES:
NA.77
PubChem Substance ID:
UNSPSC Code:
12352106
MDL number:
产品名称
5-羟基癸酸 钠盐, ≥97% (HPLC)
InChI
1S/C10H20O3.Na/c1-2-3-4-6-9(11)7-5-8-10(12)13;/h9,11H,2-8H2,1H3,(H,12,13);/q;+1/p-1
SMILES string
[Na+].CCCCCC(O)CCCC([O-])=O
InChI key
YNAGNECWEKMWRM-UHFFFAOYSA-M
assay
≥97% (HPLC)
form
powder
storage condition
desiccated
color
white to beige
solubility
H2O: 10 mg/mL, clear
Quality Level
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, type N95 (US)
Asger Andersen et al.
Cardiology, 123(3), 177-180 (2012-11-07)
We investigated whether ischemic preconditioning (IPC) protects the right ventricular (RV) myocardium against ischemic injury in hearts treated with the specific mitochondrial ATP-sensitive potassium (K(ATP)) channel blocker 5-hydroxydecanoate (5-HD). Hearts from male Wistar rats (300 g, n = 39) were
Germán A Colareda et al.
The Journal of pharmacy and pharmacology, 70(9), 1174-1187 (2018-06-23)
Low-flow ischemia (LFI) is consequent to coronary disease and produces cardiac stunning during reperfusion (R). Energetic performance and mechanisms of Ca2+ handling during LFI/R are not known. Moreover, cardioprotection of the phytoestrogen genistein (Gen) remains to be demonstrated in LFI/R.
Pinkee Phukon et al.
Biotechnology letters, 35(4), 607-611 (2012-12-25)
Using a new isolate of Pseudomonas aeruginosa, we obtained 7 g cell dry wt (CDW/l) using 5 % (w/v) glucose. Crude polyhydroxyalkanoates were obtained at 14.6 % of CDW. FTIR and NMR analysis confirmed that this was a new co-polymer:
Ischemia reperfusion injury, KATP channels, and exercise-induced cardioprotection against apoptosis.
John C Quindry et al.
Journal of applied physiology (Bethesda, Md. : 1985), 113(3), 498-506 (2012-06-02)
Exercise is a potent stimulus against cardiac ischemia reperfusion (IR) injury, although the protective mechanisms are not completely understood. The study purpose was to examine whether the mitochondrial or sarcolemmal ATP-sensitive potassium channel (mito K(ATP) or sarc K(ATP), respectively) mediates
Zhang-Feng Wang et al.
Basic research in cardiology, 108(1), 318-318 (2012-12-04)
Postconditioning (Postcon) reduces infarct size. However, its role in modulation of cardiac repair after infarction is uncertain. This study tested the hypothesis that Postcon inhibits adverse cardiac repair by reducing degradation of extracellular matrix (ECM) and synthesis of collagens via
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