Fura-2 (sodium salt)
目录号 : GC43712
A ratiometric fluorescent calcium indicator
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >90.00%
- 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. 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.
| Cas No. | SDF | ||
| 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.[Na+].[Na+].[Na+].[Na+].[Na+] | ||
| 分子式 | C29H22N3O14•5Na | 分子量 | 751.5 |
| 溶解度 | Water: 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 | 1.3307 mL | 6.6534 mL | 13.3067 mL |
| 5 mM | 0.2661 mL | 1.3307 mL | 2.6613 mL |
| 10 mM | 0.1331 mL | 0.6653 mL | 1.3307 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。
Effect of dietary sodium intake on intracellular calcium in lymphocytes of salt-sensitive hypertensive patients
Am J Hypertens 1992 Aug;5(8):536-41.PMID:1327000DOI:10.1093/ajh/5.8.536.
High dietary Na+ raises mean arterial pressure (MAP) by more than 10% in salt-sensitive (SS) patients with essential hypertension. To test whether the rise in MAP in these patients is caused by a Na(+)-linked increase in [Ca2+]i in vascular smooth muscle cells, we measured [Ca2+]i in the lymphocytes of 14 patients with essential hypertension kept on a Na+ intake of 20 mEq/day for 9 days, and 200-mEq/day for 14 days. Nifedipine gastrointestinal transport system (GITS) (30 mg/day) was given during the last 4 days of each diet. We isolated lymphocytes on Ficoll-Hypaque gradient and measured [Ca2+]i levels using Fura-2 fluorescent dye. During low Na+ intake, there was no difference in MAP (102 +/- 3.5 v 93 +/- 3.8 mm Hg) and in lymphocytes [Ca2+]i (80 +/- 3.0 v 87 +/- 5.4 nmol/L) between the seven salt-sensitive and the seven salt-resistant patients. During high Na+ intake, MAP (92 +/- 2.8 mm Hg) and [Ca2+]i (85 +/- 6.8 nmol/L) did not change in salt-resistant patients. On the contrary, MAP (115 +/- 3.4 mm Hg) and [Ca2+]i (130 +/- 11.1 nmol/L) increased significantly (P less than .01) in the salt-sensitive patients. Nifedipine did not significantly alter MAP and [Ca2+]i in both groups of patients during low Na+ and in salt-resistant patients during high Na+ intake. On the contrary, during high Na+ intake, nifedipine decreased significantly (P less than .01) both MAP (104 +/- 2.4 mm Hg) and [Ca2+]i (89 +/- 5.7 nmol/L) in salt-sensitive patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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.
Determination of cytosolic Mg2+ activity and buffering in BC3H-1 cells with mag-fura-2
Mol Cell Biochem 1994 Jul 13;136(1):11-22.PMID:7854327DOI:10.1007/BF00931599.
The magnesium buffer coefficient (BMg) was calculated for BC3H-1 cells from the rise in cytosolic Mg2+ activity observed when magnesium was released from ATP after iodoacetate (IAA) and NaCN treatment. The basal cytosolic Mg2+ activity (0.54 +/- 0.1 mM) measured with mag-fura-2 doubled when 4.54 mM magnesium was liberated from ATP: BMg was 12.9 indicating that a 1 mM increase in Mg2+ activity requires an addition of about 13 mM magnesium. The accuracy of this value depends on these assumptions: (a) all of the magnesium released from ATP stayed in the cells; (b) the rise in Mg2+ was not secondary to pH-induced changes in BMg; (c) mag-fura-2 measured Mg2+ and not Ca2+; and (d) the accuracy of the mag-fura-2 calibration. Total magnesium did not change in response to IAA/CN treatment, thus the change in Mg2+ activity reflected a redistribution of cell magnesium. pH changes induced by NH4Cl pulse and removal had little effect on Mg2+ activity and the changes were slower than and opposite to pH-induced changes in Ca2+ activity measured by Fura-2. Ca2+ responses were temporally uncoupled from Mg2+ responses when the cells were treated with IAA only and in no cases did Ca2+ levels rise above 1 microM, showing that the mag-fura-2 is responding to Mg2+. Additional studies demonstrated that approximately 90% of the mag-fura-2 signal was cytosolic in origin. The remaining non-diffusible mag-fura-2 either was bound to cytosolic membranes or sequestered in organelles with the fluorescence characteristics of the Mg2(+)-complexed form, even when cytosolic free Mg2+ activity was approximately 0.5 mM. This bound mag-fura-2 would appear to increase the Kd and thus clearly limits the accuracy of our estimmate for BMg. Despite this limitation, we demonstrate that Mg2+ is tightly regulated in face of large changes in extracellular Mg2+, and that interplay observed between pH, Ca2+ and Mg2+ activities strongly supports the hypothesis that these factors interact through a shared buffer capacity of the cell.
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.
Ca(2+)-induced inhibition of sodium pump: effects on energetic metabolism of mouse diaphragm tissue
Gen Physiol Biophys 1998 Sep;17(3):271-83.PMID:9834848doi
Tissues of mouse diaphragms were incubated in Liley solution containing 2, 4, 6 and 10 mmol/l calcium. When diaphragm tissue was incubated in 10 mmol/l calcium, an increase of intracellular calcium concentration from 314 +/- 28 to 637 +/- 26 nmol/l was estimated by fluorescent Ca2+ indicator Fura-2/AM. Moreover, incubation of the tissue in 10 mmol/l Ca2+ led to complete inhibition of electrogenic activity of the sodium pump, as measured by intracellular microelectrodes in a single muscle cell. This inhibition was fully reversible after 5 min washing with Liley solution containing 2 mmol/l CaCl2. The Ca(2+)-induced blocking effect on electrogenic activity of the sodium pump was accompanied by inhibition of glucose incorporation into the muscle tissue. Calcium at concentrations of 6 and 10 mmol/l in bath medium significantly inhibited both CO2 production and O2 consumption. A continual decrease of respiration (CO2/O2) quotient was observed under increasing concentrations of calcium. Moreover, an exponential decrease of ATP tissue levels was observed at increasing concentrations of calcium in the bath medium. On the other hand, massive acceleration of anaerobic glycolysis induced by incubation of the tissue in a medium containing high calcium concentration is improbable. This may be deduced from the fact that only about an 50% increase of lactate content in muscle tissue was observed when diaphragms were incubated for 30 min in medium containing calcium ions at 6 and 10 mmol/l as compared with the control tissue incubated for the same time in the medium containing 2 mmol/l CaCl2. In conclusion it could be stressed that increase of Ca2+ concentration in bath medium induced in diaphragm muscle tissue an elevation of intracellular Ca2+ concentration accompanied by a depression of sodium pump electrogenic activity and a depression of energy metabolism. These changes may be involved in pathology of muscle tissue during the Ca2+ overload.