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N-acetyl-L-Cysteine amide
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。
N-acetyl-L-Cysteine amide图片
CAS NO:38520-57-9
规格:98%
分子量:162.2
包装与价格:
包装价格(元)
5mg电议
10mg电议
25mg电议
50mg电议

产品介绍
N-acetyl-L-Cysteine amide (NACA) is an antioxidant.
CAS:38520-57-9
分子式:C5H10N2O2S
分子量:162.2
纯度:98%
存储:Store at -20°C

Background:

N-Acetylcysteine amide is a cell membranes and blood brain barrier permeant thiol antioxidant and neuroprotective agent, reduces ROS production.


N-Acetylcysteine amide shows no obvious effect on the viability of H9c2 cells treated with doxorubicin (DOX) at< 1 mM, but causes significant cytotoxicity at 10-20 mM. N-Acetylcysteine amide (750 μM) reduces the ROS levle and lipid peroxidation induced by DOX, and restores GSH/GSSG ratio and activities of antioxidant enzymes, such as catalase (CAT), gluthathione peroxidase (GPx), gluthathione reductase (GR)[1]. N-Acetylcysteine amide (1 mM) protects the human brain microvascular endothelial (HBMVEC) from methamphetamine (METH)- induced cell death[3].


N-Acetylcysteine amide has increased CNS bioavailability. N-Acetylcysteine amide (150 mg/kg, i.p.) improves cortical sparing and functional outcome, reduces oxidative stress, improves mitochondrial bioenergetics, and maintains mitochondrial glutathione content following traumatic brain injury (TBI) in rats[2].


参考文献:
[1]. Shi R, et al. N-acetylcysteine amide decreases oxidative stress but not cell death induced by doxorubicin in H9c2 cardiomyocytes. BMC Pharmacol. 2009 Apr 15;9:7.
[2]. Pandya JD, et al. N-acetylcysteine amide confers neuroprotection, improves bioenergetics and behavioral outcome following TBI. Exp Neurol. 2014 Jul;257:106-13.
[3]. Zhang X, et al. N-Acetylcysteine amide protects against methamphetamine-induced oxidative stress and neurotoxicity in immortalized human brain endothelial cells. Brain Res. 2009 Jun 12;1275:87-95.