BODIPY 558/568 C12
(Synonyms: Red C12) 目录号 : GC42961A fluorescent probe for lipid droplets
Cas No.:158757-84-7
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
BODIPY 558/568 C12 is a fatty acid-conjugated fluorescent probe for lipid droplets. [1] [2] It displays excitation/emission maxima of 558/568 nm, respectively, and has been used to monitor the localization and dynamics of lipid droplets in live cells.
Reference:
[1]. Targett-Adams, P., Chambers, D., Gledhill, S., et al. Live cell analysis and targeting of the lipid droplet-binding adipocyte differentiation-related protein. J. Biol. Chem. 278(18), 15998-16007 (2003).
[2]. Rambold, A.S., Cohen, S., and Lippincott-Schwartz, J. Fatty acid trafficking in starved cells: Regulation by lipid droplet lipolysis, autophagy, and mitochondrial fusion dynamics. Dev. Cell. 32(6), 678-692 (2015).
| Cas No. | 158757-84-7 | SDF | |
| 别名 | Red C12 | ||
| 化学名 | (T-4)-difluoro[5-[[5-(2-thienyl)-2H-pyrrol-2-ylidene-κN]methyl]-1H-pyrrole-2-dodecanoato(2-)-κN1]-borate(1-), monohydrogen | ||
| Canonical SMILES | [F-][B+3]1([N]2=C(C3=CC=CS3)C=CC2=CC4=CC=C(CCCCCCCCCCCC([O-])=O)[N-]14)[F-].[H+] | ||
| 分子式 | C25H30BF2N2O2S•H | 分子量 | 472.4 |
| 溶解度 | Soluble in DMSO, or in DMF | 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 | 2.1169 mL | 10.5843 mL | 21.1685 mL |
| 5 mM | 0.4234 mL | 2.1169 mL | 4.2337 mL |
| 10 mM | 0.2117 mL | 1.0584 mL | 2.1169 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。
Evaluation of in situ generated valproyl 1-O-β-acyl glucuronide in valproic acid toxicity in sandwich-cultured rat hepatocytes
Drug Metab Dispos 2014 Nov;42(11):1834-42.PMID:25147275DOI:10.1124/dmd.114.059352.
Acyl glucuronides are reactive electrophilic metabolites implicated in the toxicity of carboxylic acid drugs. Valproyl 1-O-β-acyl glucuronide (VPA-G), which is a major metabolite of valproic acid (VPA), has been linked to the development of oxidative stress in VPA-treated rats. However, relatively little is known about the toxicity of in situ generated VPA-G and its contribution to VPA hepatotoxicity. Therefore, we investigated the effects of modulating the in situ formation of VPA-G on lactate dehydrogenase (LDH) release (a marker of necrosis), BODIPY 558/568 C12 accumulation (a marker of steatosis), and cellular glutathione (GSH) content in VPA-treated sandwich-cultured rat hepatocytes. VPA increased LDH release and BODIPY 558/568 C12 accumulation, whereas it had little or no effect on total GSH content. Among the various uridine 5'-diphospho-glucuronosyltransferase inducers evaluated, β-naphthoflavone produced the greatest increase in VPA-G formation. This was accompanied by an attenuation of the increase in BODIPY 558/568 C12 accumulation, but did not affect the change in LDH release or total GSH content in VPA-treated hepatocytes. Inhibition of in situ formation of VPA-G by borneol was not accompanied by substantive changes in the effects of VPA on any of the toxicity markers. In a comparative study, in situ generated diclofenac glucuronide was not toxic to rat hepatocytes, as assessed using the same chemical modulators, thereby demonstrating the utility of the sandwich-cultured rat hepatocyte model. Overall, in situ generated VPA-G was not toxic to sandwich-cultured rat hepatocytes, suggesting that VPA glucuronidation per se is not expected to be a contributing mechanism for VPA hepatotoxicity.