您好,欢迎来到化工原料网! [登录] [免费注册]
化工原料网
位置:首页 > 产品库 > Melatonin
立即咨询
咨询类型:
     
*姓名:
*电话:
*单位:
Email:
*留言内容:
请详细说明您的需求。
*验证码:
 
Melatonin
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
Melatonin图片
CAS NO:73-31-4
规格:≥98%
包装与价格:
包装价格(元)
1g电议
2g电议
5g电议
10g电议
25g电议

产品介绍
理化性质和储存条件
Molecular Weight (MW)232.28
FormulaC13H16N2O2
CAS No.73-31-4
Storage-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)DMSO: 47 mg/mL (202.3 mM)
Water: <1 mg/mL
Ethanol: 47 mg/mL (202.3 mM)
Other info

Chemical Name: N-[2-(5-methoxy-1H-indol-3-yl)ethyl]acetamide

InChi Key: DRLFMBDRBRZALE-UHFFFAOYSA-N

InChi Code: InChI=1S/C13H16N2O2/c1-9(16)14-6-5-10-8-15-13-4-3-11(17-2)7-12(10)13/h3-4,7-8,15H,5-6H2,1-2H3,(H,14,16)

SMILES Code: CC(=O)NCCC1=CNC2=C1C=C(C=C2)OC

Synonyms

Melatonin; Melatonine; N-Acetyl-5-methoxytryptamine; Circadin; 5-Methoxy-N-acetyltryptamine; NSC 56423; NSC 113928; Regulin

实验参考方法
In Vitro

In vitro activity: Melatonin interacts with the highly toxic hydroxyl radical with a rate constant equivalent to that of other highly efficient hydroxyl radical scavengers. Melatonin reportedly neutralizes hydrogen peroxide, singlet oxygen, peroxynitrite anion, nitric oxide and hypochlorous acid. Melatonin is believed to scavenge the highly toxic hydroxyl radical, the peroxynitrite anion, and possibly the peroxyl radical. Melatonin reportedly scavenges the superoxide anion radical and it quenches singlet oxygen. Melatonin stimulates mRNA levels for superoxide dismutase and the activities of glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase (all of which are antioxidative enzymes), thereby increasing its antioxidative capacity. Melatonin in cell-free systems has been shown to directly scavenge H2O2, singlet oxygen (1O2) and nitric oxide (NO*), with little or no ability to scavenge the superoxide anion radical (O2*-) in vitro. Melatonin also directly detoxifies the peroxynitrite anion (ONOO-) and/or peroxynitrous acid (ONOOH), or the activated form of this molecule, ONOOH*. Melatonin acts as a direct free radical scavenger with the ability to detoxify both reactive oxygen and reactive nitrogen species. Melatonin inhibits cAMP accumulation in most of the cells examined, but the indole effects on other messengers have been often observed only in one type of the cells or tissue, until now. Melatonin also regulates the transcription factors, namely, phosphorylation of cAMP-responsive element binding protein and expression of c-Fos.

In VivoMelatonin increases the levels of activated PTEN, RSK-1, mTOR and AMPKα kinases, mildly inhibits ERK-1/2 phosphorylation and Bad phosphorylation, significantly inhibits phosphorylations of S6 Ribosomal Protein, 4E-BP1, GSK-3α and GSK-3β, and slightly increases PRAS40 phosphorylation in animals. Melatonin ameliorates the neurotoxiciy and astrocyte activation induced by Aβ1-42 in the cerebral cortex. Melatonin also blocks the reduction in Reelin and Dab1 expression induced by Aβ1-42. Melatonin treatment and lack of NLRP3-/- share similar inhibition of NF-κB and NLRP3 signaling pathway in mice. Melatonin treatment and lack of NLRP3-/- share some patterns of clock genes expression, and improve cardiomyocytes morphology in mice.
Animal modelMice
Formulation & DosageA total of two sets of adult male C57BL/6j mice weighing 21-26 g are randomly assigned to one of four groups and treated with intraperitoneal (i.p.) delivery of (i) vehicle (50 μL isotonic saline/5% ethanol), (ii) melatonin (4 mg/kg, dissolved in 0.9% isotonic saline/5% ethanol), (iii) Wortmannin, and (iv) melatonin/Wortmannin immediately after reperfusion. In the first set, mice are exposed to 30 min of focal cerebral ischemia (FCI) and 72 h reperfusion for the evaluation of disseminate ischemic injury in the striatum, and signaling pathway analysis (n=7 per group). The second group of mice is exposed to 90 min of FCI and 24 h reperfusion for the analysis of infarct development, brain swelling and IgG extravasation (n=7 per group).
References

J Biomed Sci. 2000 Nov-Dec;7(6):444-58; Prog Neurobiol. 1998 Oct;56(3):359-84.