12-hydroxy Lauric Acid
(Synonyms: 端羟基12酸) 目录号 : GC45962A hydroxylated fatty acid
Cas No.:505-95-3
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
12-hydroxy Lauric acid is a hydroxylated fatty acid that has been found in honey bee royal jelly.1 It is active against S. aureus, B. subtilis, B. cereus, E. coli, and P. aeruginosa bacteria (MICs = 6.25-125 μg/ml) and the fungus C. albicans (MIC = 15.63 μg/ml).
|1. Isidorov, W., Witkowski, S., Zambrzycka, M., et al. Royal jelly aliphatic acids contribute to antimicrobial activity of honey. J. Apic. Sci. 62(1), 111-123 (2018).
Cas No. | 505-95-3 | SDF | |
别名 | 端羟基12酸 | ||
Canonical SMILES | OCCCCCCCCCCCC(O)=O | ||
分子式 | C12H24O3 | 分子量 | 216.3 |
溶解度 | DMF: 3mg/mL,DMSO: 10mg/mL,Ethanol: 15mg/mL,Ethanol:PBS (pH 7.2) (1:5): 0.16mg/mL | 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 | |||
1 mg | 5 mg | 10 mg | |
1 mM | 4.6232 mL | 23.116 mL | 46.2321 mL |
5 mM | 0.9246 mL | 4.6232 mL | 9.2464 mL |
10 mM | 0.4623 mL | 2.3116 mL | 4.6232 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。
Smooth muscle--specific expression of CYP4A1 induces endothelial sprouting in renal arterial microvessels
Circ Res 2004 Feb 6;94(2):167-74.PMID:14670847DOI:10.1161/01.RES.0000111523.12842.FC.
Cytochrome P450 (CYP) 4A1 has been characterized as the most efficient arachidonic acid omega-hydroxylase catalyzing the formation of 20-hydroxyeicosatetraenoic acid (20-HETE), a potent constrictor of the renal and cerebral microcirculation and a mitogen for smooth muscle cells. We constructed adenoviruses expressing the CYP4A1 cDNA or LacZ under the control of the smooth muscle cell-specific promoter SM22alpha (Ad-SM22-4A1 and Ad-SM22-nLacZ, respectively). Beta-galactosidase expression was detected in Ad-SM22-nLacZ-transduced vascular smooth muscle A7r5 and PAC1 cells, but not in Ad-SM22-nLacZ-transduced 3T3 fibroblasts or vascular endothelial cells. Likewise, CYP4A1 mRNA and protein were detected in Ad-SM22-4A1-transduced A7r5 and PAC1 cells. Ad-SM22-4A1-transduced A7r5 cells metabolized lauric acid to 12-hydroxy-lauric acid at a rate 5 times greater than that of cells transduced with Ad-SM22-nLacZ (4.79+/-1.77 versus 0.97+/-0.57 nmol 12-hydroxy Lauric Acid/10(6) cells per h). Smooth muscle-specific LacZ expression was also detected in microdissected renal interlobar arteries transduced with Ad-SM22-nLacZ. Arteries transduced with Ad-SM22-4A1 produced higher levels of 20-HETE (4.04+/-0.29 and 13.43+/-2.84 ng/mg protein in Ad-SM22-nLacZ-transduced and Ad-SM22-4A1-transduced arteries, respectively) and demonstrated a marked angiogenic activity measured as the total length of sprouting neovessels (12.63+/-3.66 mm in Ad-SM22-4A1-transduced vessels versus 1.79+/-0.89 mm in Ad-SM22-nLacZ-transduced vessels). This angiogenic activity represented endothelial cell sprouting and was fully blocked by treatment with HET0016, a selective inhibitor of CYP4A-catalyzed reactions. The inhibitory effect of HET0016 was reversed by addition of a 20-HETE agonist. We conclude that Ad-SM22-4A1 drives a smooth muscle-specific functional expression of CYP4A1 and demonstrates increased angiogenesis, presumably via increased production of 20-HETE.
Starvation effect on rat kidney peroxisomal and microsomal fatty acid oxidation. A comparative study between liver and kidney
FEBS Lett 1993 May 3;322(1):61-4.PMID:8482369DOI:10.1016/0014-5793(93)81111-c.
Microsomal lauric acid 12-hydroxy Lauric Acid (omega)-hydroxylation and fatty acid peroxisomal beta-oxidation were studied in kidney tissue from starved rats. Starvation increased the microsomal omega-hydroxylation and peroxisomal beta-oxidation of fatty acids with a high correlation between both processes. Earlier, we reported similar results in liver. Our results support the hypothesis that the role of microsomal fatty acids omega-hydroxylation is the generation of substrate for peroxisomal beta-oxidation, with the final purpose of contributing to a catabolic or gluconeogenic pathway from fatty acids.