SBFI AM
(Synonyms: Sodium-binding Benzofuran Isophthalate Acetoxymethyl ester) 目录号 : GC44876A fluorescent Na+ indicator dye
Cas No.:129423-53-6
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
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).
| 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 |
| 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 | |||
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1 mg | 5 mg | 10 mg |
| 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 |
| 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。
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.