Fura-2 (potassium salt)
(Synonyms: 2-[6-[双(羧甲基)氨基]-5-[2-[2-[双(羧甲基)氨基]-5-甲基苯氧基]乙氧基]-2-苯并呋喃基]-5-恶唑羧酸五钾盐) 目录号 : GC43711A ratiometric fluorescent calcium indicator
Cas No.:113694-64-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Fura-2 is a ratiometric fluorescent calcium indicator that can be used to detect calcium in cells. [1] It is a pentacarboxylate that displays excitation maxima of 340 and 380 nm at high and low calcium concentrations, respectively, when the emission is fixed at 510 nm, enabling determination of ratiometric measurements of calcium influx in live cells.
Reference:
[1]. Kong, S.K., and Lee, C.Y. The use of fura 2 for measurement of free calcium concentration. Biochem. Mol. Biol. Ed. 23(2), 97-98 (1995).
| Cas No. | 113694-64-7 | SDF | |
| 别名 | 2-[6-[双(羧甲基)氨基]-5-[2-[2-[双(羧甲基)氨基]-5-甲基苯氧基]乙氧基]-2-苯并呋喃基]-5-恶唑羧酸五钾盐 | ||
| 化学名 | 2-[6-[bis(carboxymethyl)amino]-5-[2-[2-[bis(carboxymethyl)amino]-5-methylphenoxy]ethoxy]-2-benzofuranyl]-5-oxazolecarboxylic acid, pentapotassium salt | ||
| Canonical SMILES | [O-]C(CN(C1=CC2=C(C=C(C3=NC=C(C([O-])=O)O3)O2)C=C1OCCOC(C=C(C)C=C4)=C4N(CC([O-])=O)CC([O-])=O)CC([O-])=O)=O.[K+].[K+].[K+].[K+].[K+] | ||
| 分子式 | C29H22N3O14•5K | 分子量 | 832 |
| 溶解度 | 1M NaOH : 10 mg/mL (12.02 mM; Need ultrasonic and warming) | 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 | 1.2019 mL | 6.0096 mL | 12.0192 mL |
| 5 mM | 0.2404 mL | 1.2019 mL | 2.4038 mL |
| 10 mM | 0.1202 mL | 0.601 mL | 1.2019 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。
Effects of the gaseous signalling molecule nitroxyl (HNO) on myenteric neurons governing intestinal motility
J Basic Clin Physiol Pharmacol 2022 Dec 2.PMID:36455291DOI:10.1515/jbcpp-2022-0233.
Objectives: The main function of myenteric neurons is the control of gut motility. As we recently showed that nitroxyl (HNO) induces intestinal smooth muscle relaxation, it was of interest to evaluate the effects of this signalling molecule on myenteric neurons in order to distinguish its properties in regard to myocytes. Methods: Myenteric neurons isolated from the ileum of 4-10 days old rats were used. HNO-induced changes in intracellular concentration of Ca2+ or membrane potential and ion currents were measured using the Ca2+-sensitive fluorescent dye Fura-2 AM or by electrophysiological whole-cell recordings, respectively. Changes in intracellular thiol groups pool were evaluated using thiol tracker violet. Angeli's salt was used as HNO donor. Results: The HNO donor Angeli's salt induced a significant increase in the cytosolic Ca2+ concentration at the concentration 50 µM and a membrane hyperpolarization from a resting membrane potential of -56.1 ± 8.0 mV to -63.1 ± 8.7 mV (n=7). Although potassium channels primarily drive membrane potential changes in these cells, outwardly rectifying potassium currents were not significantly affected by 50 µM Angeli's salt. Fast inward sodium currents were slightly but not significantly reduced by HNO. In more sensitive cells, HNO tended to reduce the pool of thiol groups. Conclusions: As in the case of smooth muscle cells, HNO causes hyperpolarization of myenteric neurons, an effect also associated with an increase in intracellular Ca2+ concentration. Pathways other than activation of potassium currents appear to drive the hyperpolarization evoked by HNO.
IL-1β augments H2S-induced increase in intracellular Ca2+ through polysulfides generated from H2S/NO interaction
Eur J Pharmacol 2018 Feb 15;821:88-96.PMID:29337193DOI:10.1016/j.ejphar.2018.01.006.
H2S has excitatory and inhibitory effects on Ca2+ signals via transient receptor potential ankyrin 1 (TRPA1) and ATP-sensitive K+ channels, respectively. H2S converts intracellularly to polysulfides, which are more potent agonists for TRPA1 than H2S. Under inflammatory conditions, changes in the expression and activity of these H2S target channels and/or the conversion of H2S to polysulfides may modulate H2S effects. Effects of proinflammatory cytokines on H2S-induced Ca2+ signals and polysulfide production in RIN14B cells were examined using fluorescence imaging with Fura-2 and SSP4, respectively. Na2S, a H2S donor, induced 1) the inhibition of spontaneous Ca2+ signals, 2) inhibition followed by [Ca2+]i increase, and 3) rapid [Ca2+]i increase without inhibition in 50% (23/46), 22% (10/46), and 17% (8/46) of cells tested, respectively. IL-1β augmented H2S-induced [Ca2+]i increases, which were inhibited by TRPA1 and voltage-dependent L-type Ca2+ channel blockers. However, IL-1β treatment did not affect [Ca2+]i increases evoked by a TRPA1 agonist or high concentration of KCl. Na2S increased intracellular polysulfide levels, which were enhanced by IL-1β treatment. A NOS inhibitor suppressed the increased polysulfide production and [Ca2+]i increase in IL-1β-treated cells. These results suggest that IL-1β augments H2S-induced [Ca2+]i increases via the conversion of H2S to polysulfides through NO synthesis, but not via changes in the activity and expression of target channels. Polysulfides may play an important role in the effects of H2S during inflammation.
Effects of amiloride and a novel diuretic, 7-chloro-2,3-dihydro-1-(2-methylbenzoyl)-4(1H)-quinolinone-4-oxime-o-su lfonic acid, potassium salt (M17055), on calcium transport in the rabbit connecting tubule
J Pharmacol Exp Ther 1993 Sep;266(3):1589-93.PMID:8396639doi
To elucidate the mechanisms of relative anticalciuric effect of a diuretic, 7-chloro-2,3-dihydro-1-(2-methylbenzoyl)-4(1H)-quinolinone-4-oxime-o-sul fonic acid, potassium salt (M17055), having sites of action on the Henle's loop plus the distal nephron segments, we measured intracellular calcium concentration ([Ca++]i) of the rabbit connecting tubule perfused in vitro by using the microscopic fluorometry with fura 2. First, we confirmed that parathyroid hormone increases [Ca++]i by a mechanism mediated by cyclic AMP. We also confirmed that the Na+/Ca++ exchanger in the basolateral membrane is essential for the extrusion of Ca++ across this membrane. In the presence of 10 nM parathyroid hormone in the bath, the elimination of Na+ from the lumen decreased [Ca++]i, supporting the view that a decrease in Na+ supply from the apical membrane enhances the Na+/Ca++ exchanger in the basolateral membrane. Under a similar condition, the addition of 10 microM amiloride in the lumen also decreased [Ca++]i, further supporting the view that the inhibition of Na+ entry across the apical membrane causes similar effect as does Na+ elimination. Under a similar condition, the addition of 1 mM M17055 in the lumen exerted a similar effect on [Ca++]i as did amiloride. Because M17055 did not further decrease [Ca++]i when Na+ was eliminated from the lumen, the effect of M17055 is mediated by an inhibition of Na+ entry across the apical membrane. From these observations we conclude that either inhibition or diminution of Na+ entry across the apical membrane of the connecting tubule increases the Ca++ extrusion across the basolateral membrane via the Na+/Ca++ exchanger.(ABSTRACT TRUNCATED AT 250 WORDS)
Heat acclimation and heat stress have different effects on cholinergic-induced calcium mobilization
Am J Physiol Regul Integr Comp Physiol 2001 Jun;280(6):R1688-96.PMID:11353672DOI:10.1152/ajpregu.2001.280.6.R1688.
There is evidence that the signal transduction array responsible for the secretion of water in evaporative cooling by the submaxillary gland of the rat is subject to heat acclimatory responses. The objectives of the present study were 1) to examine whether heat acclimation affects intracellular Ca(2+) mobilization and, in turn, submaxillary glandular responsiveness; 2) to assess whether the acclimatory responses differ from those evoked on heat stress (HS). Experiments were conducted on submaxillary glands of rats acclimated at 34 degrees C for 0, 2 [short-term heat acclimation (STHA)], and 30 [long-term heat acclimation (LTHA)] days. The resting cytosolic calcium concentration ([Ca(2+)](c)) and the carbamylcholine-evoked calcium signal ([Ca(2+)](s)) of dispersed glandular cells were measured using the fluorescent dye fura 2 AM. Inositol-1,4,5-trisphosphate (IP(3))-sensitive endoplasmic reticulum Ca(2+) stores were determined in permeabilized cells using fura 2 potassium salt. STHA resulted in a drop in both [Ca(2+)](s) and IP(3)-sensitive Ca(2+) stores. On LTHA, the [Ca(2+)](s) amplitude reverted to the preacclimation value, whereas the IP(3)-sensitive Ca(2+) stores remained low. The drop in [Ca(2+)](s) on STHA is in accord with the decreased glandular output (measured by (86)Rb efflux) observed during this acclimation phase. However, after LTHA the enhanced glandular output despite reduced [Ca(2+)](s) levels suggests an increased efficiency of cellular secretory mechanisms in that group. Collectively, the alterations in [Ca(2+)](s) support our biphasic acclimation model (Horowitz M, Kaspler P, Marmari Y, and Oron Y. J Appl Physiol 80: 77--85, 1996.). In nonacclimated glands, HS caused an elevation in [Ca(2+)](s) coincidentally with a decrease in the IP(3) Ca(2+) stores. In contrast, [Ca(2+)](s) in both STHA and LTHA glands was not affected by HS, despite a marked increase in the IP(3)-sensitive Ca(2+) stores in the LTHA glands. The opposing responses to HS and heat acclimation in calcium signaling and stores confirm the specificity of each process.
Actions of hydrogen sulphide on ion transport across rat distal colon
Br J Pharmacol 2009 Nov;158(5):1263-75.PMID:19785650DOI:10.1111/j.1476-5381.2009.00385.x.
Background and purpose: The aim of this study was to identify the actions of H(2)S on ion transport across rat distal colon. Experimental approach: Changes in short-circuit current (Isc) induced by the H(2)S-donor, NaHS, were measured in Ussing chambers. Cytosolic Ca(2+) concentration was evaluated using Fura-2. Key results: NaHS concentration-dependently induced a change in Isc, that was only partially inhibited by the neurotoxin, tetrodotoxin. Lower concentrations (< or =10(-3) mol.L(-1)) of NaHS induced a monophasic increase in Isc, whereas higher concentrations induced an additional, secondary fall of Isc, before a third phase when Isc rose again. Blockers of H(2)S-producing enzymes (expression demonstrated immunohistochemically) decreased basal Isc, suggesting that endogenous production of H(2)S contributes to spontaneous anion secretion. The positive Isc phases induced by NaHS were due to Cl(-) secretion as shown by anion substitution and transport inhibitor experiments, whereas the transient negative Isc induced by higher concentrations of the H(2)S-donor was inhibited by mucosal tetrapentylammonium suggesting a transient K(+) secretion. When applied from the serosal side, glibenclamide, an inhibitor of ATP-sensitive K(+) channels, and tetrapentylammonium, a blocker of Ca(2+)-dependent K(+) channels, suppressed NaHS-induced Cl(-) secretion suggesting different types of K(+) channels are stimulated by the H(2)S-donor. NaHS-induced increase in cytosolic Ca(2+) concentration was confirmed in isolated, fura-2-loaded colonic crypts. This response was not dependent on extracellular Ca(2+), but was inhibited by blockers of intracellular Ca(2+) channels present on Ca(2+) storage organelles. Conclusions and implications: H(2)S induces colonic ion secretion by stimulation of apical as well as basolateral epithelial K(+) channels.