N-Acetylcysteine amide had no significant effect on the viability of doxorubicin-treated H9c2 cells at less than 1 mM, but produced significant cytotoxicity at 10-20 mM. N-Acetylcysteine amide at a concentration of 750 μM reduced doxorubicin-induced ROS concentration and lipid peroxidation, and restored the GSH/GSSG ratio and the activities of antioxidant enzymes such as catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR)[1].N-Acetylcysteine amide at a concentration of 1 mM protected human brain microvascular endothelial cells (HBMVEC) from methamphetamine-induced cell death[2].
N-acetylcysteine amide 细胞实验
Cell Line
Concentration
Treated Time
Description
References
HB1.F3.CD neural stem cells
1 mM
72 hours
To evaluate the effect of NACA on the viability of CRAd-S-pk7-loaded neural stem cells, the results showed that NACA significantly increased the viability of neural stem cells and enhanced viral replication.
Mol Ther. 2013 Nov;21(11):2063-73.
U87 glioma cells
1 mM
72 hours
To evaluate the effect of NACA on the viability of U87 glioma cells, the results showed that NACA did not significantly increase the viability of U87 cells.
Mol Ther. 2013 Nov;21(11):2063-73.
Human retinal pigment epithelial cells
1 mM
8 hours
To evaluate the effect of N-acetylcysteine amide on oxidative stress-induced microparticle release, results showed that NACA significantly reduced oxidative stress-induced microparticle release.
Invest Ophthalmol Vis Sci. 2016 Feb;57(2):360-71.
N-acetylcysteine amide 动物实验
Species
Animal Model
Administration
Dosage
Frequency
Description
References
Mice
VP-PXR transgenic mice
Intraperitoneal injection
200 mg/kg
Once, 1 hour before HS/R
NACA treatment attenuated HS-induced hepatic injury, as shown by reduced histological necrosis and decreased serum ALT levels.
Hepatology. 2019 Sep;70(3):995-1010
Nude mice
Intracranial glioma xenograft model
Intraperitoneal injection
250 mg/kg/day
Once daily for 5 days
To evaluate the effect of combined treatment of NACA and CRAd-S-pk7-loaded neural stem cells on the survival of glioma-bearing mice, the results showed that the combined treatment significantly prolonged the survival of mice and increased intratumoral viral distribution.
Mol Ther. 2013 Nov;21(11):2063-73.
CD-1 mice
HIV-associated dementia model
Intraperitoneal injection
250mg/kg
Once daily for 5 days
NACA significantly protected animals from oxidative stress-induced damage and restored BBB permeability
Free Radic Biol Med. 2010 May 15;48(10):1388-98
Drosophila melanogaster
Adult virgin female flies
Oral
300 µg/mL
5 hours
NACA treatment improved the movement and survival of larvae exposed to spinosad, indicating a causal role for oxidative stress in the mode of action of spinosad at low doses.
Elife. 2022 Feb 22;11:e73812
Drosophila
Drosophila model
Oral
40 μg/ml
Starting from 2 days and continued
NACA treatment completely rescued the climbing defects in tau RNAi flies, indicating that aberrant ROS accumulations are driving this phenotype.
Nat Neurosci. 2024 Oct;27(10):1918-1933
Wistar rats
Aβ1-42 peptide-induced Alzheimer's-like pathology model
Intraperitoneal injection
75 mg/kg
Once daily for 7 days
NACA treatment reversed cognitive deficits and reduced oxidative stress in the hippocampus and prefrontal cortex. Western blot analysis and immunohistochemistry demonstrated NACA's neuroprotective effects on neurogenesis, expression of neurofibrillary tangles, β-amyloid peptide, synaptophysin, neuronal morphology, and gliosis.
Int J Mol Sci. 2023 Aug 12;24(16):12733
Drosophila melanogaster
Drosophila larvae and adults
Supplemented in food
75 μg/mL
Continuous administration for 20 days
NACA significantly ameliorated the accumulation of LDs in the fat body, impaired larval movement and adult climbing ability, and reduced adult longevity caused by imidacloprid.
Proc Natl Acad Sci U S A. 2020 Oct 13;117(41):25840-25850
N-acetylcysteine amide 动物研究
Animal study
N-Acetylcysteine amide increases bioavailability in the central nervous system. Administered intraperitoneally at a dose of 150 mg/kg, N-Acetylcysteine amide improves cortical laxity and functional recovery, reduces oxidative stress, improves mitochondrial bioenergetics, and maintains mitochondrial glutathione levels after traumatic brain injury (TBI) in rats[3].
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