| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5g | 电议 |
| 10g | 电议 |
Preparation Method | PRP was preincubated at 37℃ for 4 min with Acetylcysteine or with nitroglycerin, or first with Acetylcysteine and then nitroglycerin, and sodium nitroprusside, sodium azide, sodium nitrite, or S-nitroso-N-acetylcysteine for 1 min before addition of agonist. |
Reaction Conditions | 5.5 mM Acetylcysteine for 4 min |
Applications | Millimolar concentrations of Acetylcysteine potentiated markedly the inhibitory effect of nitroglycerin on platelet aggregation induced by ADP, epinephrine, collagen, and arachidonate, decreasing the 50% inhibitory concentration (IC50) approximately 50-fold for each of these agents. |
Cell lines | PC12 cell line |
Preparation Method | Cells were treated with 100 ng/ml NGF or 60 mm Acetylcysteine in serum-containing medium for the indicated times. |
Reaction Conditions | 60 mm Acetylcysteine for 15min-4h |
Applications | Acetylcysteine activates the Ras-ERK pathway |
Animal models | Thirty-five male Wistar rats |
Preparation Method | Group control underwent IIR without Acetylcysteine. In the other groups, Acetylcysteine was administered intraperitoneally with different regimens: 150 mg/kg before ischemia, 300 mg/kg before ischemia, and 150 mg/kg before ischemia plus 150 mg/kg 5 min before reperfusion. |
Dosage form | 150-300 mg/kg Acetylcysteine(Intraperitoneal administration) |
Applications | Acetylcysteine exerts a significant protective role in liver injury following IIR, which seems to be independent of an intestinal protective effect. Additional administration of Acetylcysteine before reperfusion was of no further benefit. The most effective regimen among the compared regimens was that of 300 mg/kg before ischemia. |
| 产品描述 | Acetylcysteine is the N-acetyl derivative of CYSTEINE. NAC (N-acetyl-L-cysteine) is commonly used to identify and test ROS (reactive oxygen species) inducers, and to inhibit ROS.Acetylcysteine (N-Acetylcysteine) is a mucolytic agent which reduces the thickness of the mucus[1]. It has also been shown to have antiviral effects in patients with HIV due to inhibition of viral stimulation by reactive oxygen intermediates. Acetylcysteine also has anti-influenza virus activities[5]. Millimolar concentrations of Acetylcysteine potentiated markedly the inhibitory effect of nitroglycerin on platelet aggregation induced by ADP, epinephrine, collagen, and arachidonate, decreasing the 50% inhibitory concentration (IC50) approximately 50-fold for each of these agents.In the absence of Acetylcysteine, nitroglycerin induced a marked decrease in platelet-reduced glutathione content as S-nitroso-thiol adducts were produced. The synthetic S-nitroso-thiol, S-nitroso-N-acetylcysteine, markedly inhibited platelet aggregation with an IC50 of 6 nM[7].Acetylcysteine increased ERK-1 activity in PC12 cells after 15 min of treatment and maximal stimulatory activity for 60 min. We also observed that Acetylcysteine caused tyrosine phosphorylation of ERK-1 in cells treated with this compound for 30 min[4].Acetylcysteine induces cell apoptosis. When used serum-deprived PC12 cells, neuronally differentiated PC12 cells deprived of serum and NGF, and NGF-deprived neonatal sympathetic neurons. In each case L-Acetylcysteine prevents apoptotic DNA fragmentation and maintains long-term survival in the absence of other trophic support[3].Acetylcysteine prevents hemin-induced ferroptosis by neutralizing toxic lipids generated by arachidonate-dependent activity of 5-lipoxygenases[2]. In mice, Acetylcysteine exerts a significant protective role in liver injury following IIR, which seems to be independent of an intestinal protective effect. Additional administration of Acetylcysteine before reperfusion was of no further benefit. The most effective regimen among the compared regimens was that of 300 mg/kg before ischemia[6]. References: |
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