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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
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 是一种细胞膜和血脑屏障渗透硫醇抗氧化剂和神经保护剂,可减少 ROS 的产生。

Cell experiment:

To choose a sublethal concentration of N-Acetylcysteine amide and N-acetylcysteine for the study on their ability to protect cells from doxorubicin (DOX)-induced toxicity, H9c2 cells are exposed with N-Acetylcysteine amide or N-acetylcysteine at 0.25 mM, 0.50 mM, 0.75 mM, 1 mM, 2 mM, 5 mM, 10 mM, and 20 mM for 24 h. Untreated cells are used as the control for each experiment[1].

Animal experiment:

Rats[2]In order to assess mitochondrial respiration and glutathione content following traumatic brain injury (TBI), rats are randomly divided into three groups (n = 5 animals/group). (I.) N-Acetylcysteine amide group receives multiple bolus IP injections of N-Acetylcysteine amide (150 mg/kg) immediately after 5 minutes and then every 6 hours up to 24 hrs post-injury. (II.) Vehicle group receives equivalent v/v saline at 5 minutes and every 6 hours (6, 12, 18, 24 hrs) up to 24 hrs post-injury. (III.) Sham injured group animals do not receive any drug treatment. At 25 hrs post-injury, all animals are euthanized and mitochondria are isolated from the ipsilateral cortical hemisphere (6 mm punch) to carry out measurements of mitochondrial respiration and glutathione content[2].

产品描述

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].

References:
[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.