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SBFI AM

(Synonyms: Sodium-binding Benzofuran Isophthalate Acetoxymethyl ester) 目录号 : GC44876

A fluorescent Na+ indicator dye

SBFI AM Chemical Structure

Cas No.:129423-53-6

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1mg
¥6,766.00
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产品描述

SBFI AM is a membrane-permeant, fluorescent Na+ indicator dye. It is selective for Na+ over K+ with Kd values of 20 and 120 mM for these ions, respectively. [1]Increasing concentration of Na+ increases the ratio of excitation efficiency at 330-345 nm to that at 370-390 nm with emission collected at 450-550 nm. [1]  Therefore, ratio fluorometry and imaging can be performed with the same wavelengths. SBF AM is suitable for single intracellular dye injection and is typically used for high-resolution measurements of Na+ concentration in intact tissue through two-photon confocal imaging.[2]

Reference:
[1]. Minta, A., and Tsien, R.Y. Fluorescent indicators for cytosolic sodium. The Journal of Biological Chemisty 264(32), 19449-19457 (1989).
[2]. Meier, S.D., Kovalchuk, Y., and Rose, C.R. Properties of the new fluorescent Na+ indicator CoroNa Green: Comparison with SBFI and confocal Na+ imaging. Journal of Neuroscience Methods 155(2), 251-259 (2006).

Chemical Properties

Cas No. 129423-53-6 SDF
别名 Sodium-binding Benzofuran Isophthalate Acetoxymethyl ester
化学名 4,4’-[1,4,10-trioxa-7,13-diazacyclopentadecane-7,13-diylbis(5-methoxy-6,2-benzofurandiyl)]bis-1,3-benzenedicarboxylic acid 1,1’,3,3’-tetrakis[(acetyloxy)methyl] ester
Canonical SMILES O=C(OCOC(C)=O)C(C=C1)=CC(C(OCOC(C)=O)=O)=C1C2=CC(C=C3OC)=C(O2)C=C3N4CCOCCOCCN(C5=C(OC)C=C(C=C(C6=C(C(OCOC(C)=O)=O)C=C(C(OCOC(C)=O)=O)C=C6)O7)C7=C5)CCOCC4
分子式 C56H58N2O23 分子量 1127.1
溶解度 Methanol: Soluble 储存条件 Store at -20°C
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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。
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1 mM 0.8872 mL 4.4362 mL 8.8723 mL
5 mM 0.1774 mL 0.8872 mL 1.7745 mL
10 mM 0.0887 mL 0.4436 mL 0.8872 mL
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Research Update

Non-preferential fuelling of the Na(+)/K(+)-ATPase pump

Biochem J 2014 Jun 15;460(3):353-61.PMID:24665934DOI:10.1042/BJ20140003.

There is abundant evidence that glycolysis and the Na(+)/K(+)-ATPase pump are functionally coupled, and it is thought that the nature of the coupling is energetic, with glycolysis providing the ATP that fuels the pump. This notion has been instrumental to current models of brain energy metabolism. However, structural and biophysical considerations suggest that the pump should also have access to mitochondrial ATP, which is much more abundant. In the present study, we have investigated the source of ATP that fuels the Na(+) pump in astrocytes, taking advantage of the high temporal resolution of recently available FRET nanosensors for glucose, lactate and ATP. The activity of the Na(+) pump was assessed in parallel with the Na(+)-sensitive dye SBFI AM (Na(+)-binding benzofuran isophthalate acetoxymethyl ester). OXPHOS (oxidative phosphorylation) inhibition resulted in bulk ATP depletion and a 5-fold stimulation of glycolytic flux, in spite of which Na(+) pumping was inhibited by 90%. Mathematical modelling of ATP dynamics showed that the observed pump failure is inconsistent with preferential fuelling of the Na(+) pump by glycolytic ATP. We conclude that the nature of the functional coupling between the Na(+) pump and the glycolytic machinery is not energetic and that the pump is mainly fuelled by mitochondrial ATP.

Two mechanisms involved in trigeminal CGRP release: implications for migraine treatment

Headache 2013 Jan;53(1):67-80.PMID:23095108DOI:10.1111/j.1526-4610.2012.02262.x.

Objective/background: The goal of this study was to better understand the cellular mechanisms involved in proton stimulation of calcitonin gene-related peptide (CGRP) secretion from cultured trigeminal neurons by investigating the effects of 2 antimigraine therapies, onabotulinumtoxinA and rizatriptan. Stimulated CGRP release from peripheral and central terminating processes of trigeminal ganglia neurons is implicated in migraine pathology by promoting inflammation and nociception. Based on models of migraine pathology, several inflammatory molecules including protons are thought to facilitate sensitization and activation of trigeminal nociceptive neurons and stimulate CGRP secretion. Despite the reported efficacy of triptans and onabotulinumtoxinA to treat acute and chronic migraine, respectively, a substantial number of migraineurs do not get adequate relief with these therapies. A possible explanation is that triptans and onabotulinumtoxinA are not able to block proton-mediated CGRP secretion. Methods: CGRP secretion from cultured primary trigeminal ganglia neurons was quantitated by radioimmunoassay while intracellular calcium and sodium levels were measured in neurons via live cell imaging using Fura-2 AM and SBFI AM, respectively. The expression of acid-sensing ion channel 3 (ASIC3) was determined by immunocytochemistry and Western blot analysis. In addition, the involvement of ASICs in mediating proton stimulation of CGRP was investigated using the potent and selective ASIC3 inhibitor APETx2. Results: While KCl caused a significant increase in CGRP secretion that was significantly repressed by treatment with ethylene glycol tetraacetic acid (EGTA), onabotulinumtoxinA, and rizatriptan, the stimulatory effect of protons (pH 5.5) was not suppressed by EGTA, onabotulinumtoxinA, or rizatriptan. In addition, while KCl caused a transient increase in intracellular calcium levels that was blocked by EGTA, no appreciable change in calcium levels was observed with proton treatment. However, protons did significantly increase the intracellular level of sodium ions. Under our culture conditions, ASIC3 was shown to be expressed in most trigeminal ganglion neurons. Importantly, proton stimulation of CGRP secretion was repressed by pretreatment with the ASIC3 inhibitor APETx2, but not the transient receptor potential vanilloid-1 antagonist capsazepine. Conclusions: Our findings provide evidence that proton regulated release of CGRP from trigeminal neurons utilizes a different mechanism than the calcium and synaptosomal-associated protein 25-dependent pathways that are inhibited by the antimigraine therapies, rizatriptan and onabotulinumtoxinA.