Indo-1 (sodium salt)
目录号 : GC43900A 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
Indo-1 is a ratiometric fluorescent calcium indicator. It is ideal for analyses using flow cytometry, as it uses a single excitation source, typically 349-364 nm light from an argon-ion laser. The emission maximum shifts from 475-485 nm without calcium to 400-410 nm when indo-1 binds calcium. Indo-1 is prone to photobleaching, which limits its usefulness in methods involving microscopy.
| Cas No. | SDF | ||
| Canonical SMILES | [O-]C(CN(CC([O-])=O)C1=CC=C(C2=CC3=C(C=C(C([O-])=O)C=C3)N2)C=C1OCCOC4=C(N(CC([O-])=O)CC([O-])=O)C=CC(C)=C4)=O.[Na+].[Na+].[Na+].[Na+].[Na+] | ||
| 分子式 | C32H26N3O12•5Na | 分子量 | 759.5 |
| 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 | 1.3167 mL | 6.5833 mL | 13.1666 mL |
| 5 mM | 0.2633 mL | 1.3167 mL | 2.6333 mL |
| 10 mM | 0.1317 mL | 0.6583 mL | 1.3167 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。
The fluorescent calcium indicator Indo-1/AM inhibits renal proximal tubule cell volume regulation
Ann Clin Lab Sci 1992 Jul-Aug;22(4):236-44.PMID:1503391doi
The intracellular calcium indicator, Indo-1, is a fluorescent compound related in structure and function to the calcium chelator ethylene glycol-bis(beta-aminoethyl ether) tetraacetic acid (EGTA) that binds one calcium ion per molecule. In the extracellular range of 1 to 10 microM Indo-1/AM, the estimated intracellular concentration of the dye is 0.1 to 3 microM. Therefore, it is likely that intracellular calcium signals could be blunted under these experimental conditions (Cai approximately 0.1 to 0.2 microM). To evaluate the potential effects of Indo-1/AM on cellular function, proximal renal tubules of the teleost Carassius auratus (goldfish) were exposed to its acetoxymethyl ester (cell permeable form) in an isotonic Ringer's solution (290 mOsm, 0.1 mM calcium) followed by exposure to a low sodium hypotonic Ringer's (110 mOsm, 0.1 mM calcium). Cellular regulatory volume decreases (RVD) were determined with videometric methods. In proximal renal tubules incubated with Indo-1/AM, RVD was inhibited in a dose-dependent fashion (3 to 5 microM). No effects on RVD were observed with the impermeant salt of Indo-1. Overt cellular injury was found at 10 microM Indo-1/AM as evidenced by mitochondrial and cell swelling, cellular detachment from the tubular basement membrane, and different degrees of cytolysis. It is postulated by us that the inhibitory effects of Indo-1/AM (3-5 microM) on RVD are due to intracellular calcium chelation followed by disruption of intracellular signalling.
Detection of La3+ influx in ventricular cells by Indo-1 fluorescence
Am J Physiol 1989 Feb;256(2 Pt 1):C351-7.PMID:2919662DOI:10.1152/ajpcell.1989.256.2.C351.
We exposed indo-1-loaded cultured embryonic chick ventricular cells to 0.03-1.0 mM extracellular lanthanum concentration ([La3+]o) and simultaneously measured cell contractile motion and the 410/480 nm fluorescence intensity ratio. After exposure to La3+, ventricular cells stopped contracting and relaxed within seconds, and the 410/480 fluorescence ratio increased. The increase in the 410/480 signal was related to [La3+]o but was not affected by short exposures to zero extracellular calcium concentration ([Ca2+]o) or caffeine, suggesting that the fluorescence was not caused by a La3+-induced increase in intracellular calcium concentration ([Ca2+]i) but rather to increased intracellular lanthanum concentration ([La3+]i). In vitro studies confirmed that Indo-1 fluorescence was sensitive to La3+. The increase in [La3+]i in 0.1 mM [La3+]o was directly related to intracellular sodium concentration ([Na+]i), suggesting that La3+ entered cells via Na+-La3+ exchange. In contrast to ventricular cells, which have a functionally distinct Na+-Ca2+ exchange system, exposure of indo-1-loaded cultured bovine endothelial cells to La3+ failed to produce an increase in [La3+]i. These results indicate that exposure of ventricular cells to 0.1-1.0 mM [La3+]o results in a [La3+]i greater than 250 nM within 1 min. Therefore, changes in myocardial 45Ca2+ fluxes and contents induced by La3+ cannot be ascribed solely to extracellular La3+ effects.
Protein kinase inhibitors reduce SR Ca transport in permeabilized cardiac myocytes
Am J Physiol 1994 Aug;267(2 Pt 2):H812-20.PMID:8067437DOI:10.1152/ajpheart.1994.267.2.H812.
Phosphorylation of the sarcoplasmic reticulum (SR) protein phospholamban by adenosine 3',5'-cyclic monophosphate (cAMP)-dependent protein kinase (PKA) and Ca-calmodulin-dependent protein kinase (CaM-KII) stimulates Ca-adenosinetriphosphatase (ATPase) activity and SR Ca transport, but the role of CaM-KII-dependent phosphorylation is not well defined. We studied the PKA- and CaM-KII-dependent regulation of SR Ca transport in digitonin-permeabilized rabbit ventricular myocytes. SR Ca uptake and free Ca concentration were measured on line with indo 1 and Ca electrodes in the presence of 20 microM ruthenium red and 10 mM oxalate. neither N5,2'-w-dibutyryl-cAMP (up to 500 microM) nor the nonhydrolyzable cAMP agonist adenosine 3'5'-cyclic monophosphorothioate sodium salt (Sp-cAMP[S]; up to 275 microM) affected the maximum uptake rate (Vmax) or the dissociation constant (Kd) for Ca uptake. However, the PKA inhibitor H-89 significantly increased Kd (e.g., from 307 +/- 67 to 826 +/- 62 nM Ca at 40-65 microM H-89) without significantly affecting Vmax. Both CaM-KII inhibitors, KN-62 (60 microM) and a CaM-KII inhibitory peptide (10 microM), significantly decreased Vmax from 11.95 +/- 0.5 to 9.48 +/- 0.6 nmol.mg-1.min-1 and from 10.95 +/- 1.72 to 7.37 +/- 0.94 nmol.mg-1.min-1, respectively, without consistently changing Kd. The effects of H-89 on Kd and of KN-62 on Vmax were prevented by a monoclonal antibody to phospholamban 2D12 (consistent with the antibody removing the inhibitory effect of phospholamban on the SR Ca-ATPase).(ABSTRACT TRUNCATED AT 250 WORDS)
Nitric oxide stimulates Ca(2+)-independent synaptic vesicle release
Neuron 1994 Jun;12(6):1235-44.PMID:7912090DOI:10.1016/0896-6273(94)90440-5.
A new fluorescence method using the dye FM1-43 was used to examine exocytotic release from hippocampal synaptosomes. Nitric oxide caused a marked transient stimulation of vesicle release. Several structurally unrelated nitric oxide donors, sodium nitroprusside, S-nitroso-N-acetylpenicillamine, 3-morpholino-sydnonimine, and acidified sodium nitrite, were effective. Release stimulated by nitric oxide and KCl were comparable in time course, using both the fluorescence assay and [3H]L-glutamate to monitor neurotransmitter release. Activation of guanylyl cyclase was not responsible for nitric oxide-stimulated release. Unlike release stimulated by KCl or A23187, nitric oxide-stimulated release was found to be independent of a rise in intrasynaptosomal Ca2+. Indo-1/AM measurements indicated that nitric oxide actually decreased intracellular Ca2+, and the Ca2+ channel blocker Cd2+ did not affect nitric oxide-stimulated vesicle release. Nitric oxide does, however, appear to act on the Ca(2+)-sensitive pool of vesicles. Nitric oxide may be the first physiological mediator that induces vesicle exocytosis without raising Ca2+ and may provide an interesting new tool for the study of molecules involved in vesicle exocytosis.
Inhibition of Na+ channels ameliorates arrhythmias in a drug-induced model of Andersen-Tawil syndrome
Heart Rhythm 2013 Feb;10(2):255-63.PMID:23041575DOI:10.1016/j.hrthm.2012.10.005.
Background: Andersen-Tawil syndrome (ATS1)-associated ventricular tachycardias (VTs) are initiated by frequent, hypokalemia-exacerbated, premature ventricular activity (PVA). We previously demonstrated that a guinea pig model of drug-induced ATS1 (DI-ATS1) evidenced increased arrhythmias from regions with high Na(+)/Ca(2+)-exchange expression. Objective: Therefore, we hypothesize that reduced cytosolic Na(+) entry through either cardiac isoform of or tetrodotoxin (TTX)-sensitive Na(+) channels during DI-ATS1 can ameliorate arrhythmia burden. Methods: DI-ATS1 was induced with 10 μM BaCl(2) and 2 mM extracellular K(+). Ca(2+) transients and conduction velocity (CV) were optically mapped with Indo-1 and di-4-ANEPPS, respectively, from Langendorff-perfused guinea pig ventricles. Results: Nonselective Na(+) channel blockade with 1 μM flecainide reduced amplitude (Ca(A)), slowed left ventricular CV, reduced tissue excitability, and abolished the incidence of VT while decreasing the incidence of PVA relative to DI-ATS1. Selective, TTX-sensitive Na(+) channel blockade with TTX (100 nM) during DI-ATS1 decreased Ca(A) and decreased the inducibility of VTs and PVA relative to DI-ATS1 without slowing CV. Ranolazine altered Ca(A), left ventricular CV, tissue excitability, and reduced inducibility of VT and PVA in a concentration-dependent manner. None of the aforementioned interventions altered diastolic Ca(2+) levels or Ca(2+) transient decay time constant. Conclusions: These data suggest that cytosolic Na(+) entry and its modulation of Ca(2+) handling are necessary for arrhythmogenesis. During the loss of inward-rectifier K(+) current function, not only Na(+)/Ca(2+)-exchange dominance but Na(+) flux may determine arrhythmia burden. Therefore, selective inhibition of TTX-sensitive Na(+) channels may offer a potential therapeutic target to alleviate arrhythmias during states of Ca(2+) overload secondary to loss of inward-rectifier K(+) current function without compromising the excitability reserve.