Acetylcysteine

CAS号

616-91-1

分子式

C5H9NO3S

主要靶点

ROS|Influenza Virus|Endogenous Metabolite|Reactive Oxygen Species|Apoptosis|TNF|Ferroptosis

仅限科研使用

Cat No : CM01020

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Synonyms

ROS|TNF-α|易咳净|乙酰半胱氨酸|N-Acetyl Cysteine|NAC|N-Acetylcysteine|N-Acetyl-L-cysteine|Reactive Oxygen Species|ReactiveOxygenSpecies|Inhibitor|inhibit|LNAC|Influenza Virus|InfluenzaVirus|EndogenousMetabolite|Ferroptosis|Endogenous Metabolite|Apoptosis|Acetylcysteine



产品信息

CAS号 616-91-1
分子式 C5H9NO3S
主要靶点 ROS|Influenza Virus|Endogenous Metabolite|Reactive Oxygen Species|Apoptosis|TNF|Ferroptosis
主要通路 代谢|免疫与炎症|微生物学|免疫与炎症|代谢|NF-κB 信号通路|凋亡|凋亡|凋亡
分子量 163.19
纯度 100%, 此纯度可做参考,具体纯度与批次有关系,可咨询客服
储存条件 keep away from moisture | Powder: -20°C for 3 years | Shipping with blue ice.
别名 ROS|TNF-α|易咳净|乙酰半胱氨酸|N-Acetyl Cysteine|NAC|N-Acetylcysteine|N-Acetyl-L-cysteine|Reactive Oxygen Species|ReactiveOxygenSpecies|Inhibitor|inhibit|LNAC|Influenza Virus|InfluenzaVirus|EndogenousMetabolite|Ferroptosis|Endogenous Metabolite|Apoptosis|Acetylcysteine

体内活性

方法:为研究对小鼠凋亡性肝损伤的影响,将 Acetylcysteine (150 mg/kg) 单次腹腔注射给 CD-1 小鼠,30 min 后 使用 GalN/LPS 诱导肝损伤。 结果:Acetylcysteine 预处理显著减轻了 GalN/LPS 诱导的肝细胞凋亡。Acetylcysteine 通过其强大的 ROS 清除和抗凋亡作用减轻 GalN/LPS 诱导的凋亡性肝损伤。[3] 方法:为检测体内活性,将 Acetylcysteine (500 mg/kg) 口服给药给亨廷顿舞蹈症 (HD)的 R6/1 转基因小鼠,每天一次,持续九周。 结果:慢性 Acetylcysteine 给药延迟了 R6/1 小鼠运动缺陷的发生和发展,同时对 R6/1 和野生型小鼠都具有抗抑郁样作用。[4]

体外活性

方法:人膀胱癌细胞 T24 用 Acetylcysteine (5-50 mM) 处理 24 h,使用 MTT 方法检测细胞活力。 结果:Acetylcysteine 剂量依赖性抑制 T24 细胞活力,IC50 为 33.33 mM。[1] 方法:大鼠心肌细胞 H9c2 用 Acetylcysteine (2-4 mM) 处理 12-24 h,使用 Flow Cytometry 方法检测细胞凋亡情况。 结果:Acetylcysteine 剂量和时间依赖性诱导 H9c2 细胞凋亡。[2]

溶解度

H2O:100 mg/ml (612.78 mM);DMSO:60 mg/mL (367.67 mM);Ethanol:31 mg/mL (190 mM)

细胞实验

For survival experiments, washed cells are resuspended in RPM1 1640 medium and plated in 0.5 mL at a density of 8-10×105 per well in 24 well plastic culture dishes coated with rat tail collagen. To feed, but to avoid loss of floating cells, fresh medium (0.2 mL) is added to the cultures on days 1, 5, and 10. For experiments involving 'primed' PC12 cells, cultures are pretreated for l-2 weeks with NGF in RPM1 1640 medium supplemented with 1% heat-iN-acetylcysteinetivated horse serum. The cells are then washed and passaged into serum-free RPM1 1640 medium.

动物实验

Rats are randomly allocated into five groups: sham group (n=5), control group with IIR (n=8) and three groups with IIR who are given N-acetylcysteine in different dosages: 150 mg/kg intraperitoneally 5 min before ischemia (n=8, group N-acetylcysteine 150), 300 mg/kg i.p 5 min before ischemia (n=7, group N-acetylcysteine 300), and 150 mg/kg i.p 5 min before ischemia plus 150 mg/kg 5 min before reperfusion (n=7, group N-acetylcysteine 150 + 150). After 4 h of reperfusion, the animals are euthanized by exsanguination from the abdominal aorta.[1]

参考文献

1.Supabphol A, et al. N-acetylcysteine inhibits proliferation, adhesion, migration and invasion of human bladder cancer cells. J Med Assoc Thai. 2009 Sep;92(9):1171-7.
2.Liu Y, et al. N?acetylcysteine induces apoptosis via the mitochondria?dependent pathway but not via endoplasmic reticulum stress in H9c2 cells. Mol Med Rep. 2017 Nov;16(5):6626-6633.
3.Wang H, et al. N-acetylcysteine attenuates lipopolysaccharide-induced apoptotic liver damage in D-galactosamine-sensitized mice. Acta Pharmacol Sin. 2007 Nov;28(11):1803-9.
4.Wright DJ, et al. N-Acetylcysteine improves mitochondrial function and ameliorates behavioral deficits in the R6/1 mouse model of Huntington's disease. Transl Psychiatry. 2015 Jan 6;5(1):e492.
5.Farr SA, et al. J Neurochem, 2003, 84(5), 1173-1183.
6.Kalimeris K, et al. N-acetylcysteine ameliorates liver injury in a rat model of intestinal ischemia reperfusion. J Surg Res. 2016 Dec;206(2):263-272.
7.Xu B, Xu J, Cai N, et al. Roflumilast prevents ischemic stroke-induced neuronal damage by restricting GSK3β-mediated oxidative stress and IRE1α/TRAF2/JNK pathway[J]. Free Radical Biology and Medicine. 2020
8.Xu B, Qin Y, Li D, et al. Inhibition of PDE4 protects neurons against oxygen-glucose deprivation-induced endoplasmic reticulum stress through activation of the Nrf-2/HO-1 pathway[J]. Redox Biology. 2020, 28: 101342.

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The dilution calculator equation

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