体外活性
体外活性/In vitro:
1.Acetylcysteine/NAC还可防⽌ PC12 细胞和交感神经元死亡[1]。
2.Acetylcysteine/NAC导致⼤⿏和⼈主动脉平滑肌细胞的活⼒呈剂量依赖性降低[2]。
3.Acetylcysteine/NAC激活 PC12 细胞中的 Ras 细胞外信号调节激酶 (ERK) 通路。Acetylcysteine/NAC保护神经元细胞免于因营养⽀持撤消⽽引起的死亡。Acetylcysteine/NAC增加⾎管组织中蛋⽩质结合储存的⼀氧化氮 (NO) 释放。Acetylcysteine/NAC预处理 PC12 细胞会⼲扰 NGF 依赖的信号传导和神经突的⽣⻓，提⽰ Acetylcysteine 会⼲扰 NGF 机制中的氧化还原敏感步骤[3]。
体内活性/In vivo:
1.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。[5]
2.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。[6]
细胞实验/Cell Research:
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.[1]
动物实验/Animal Research:
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.[4]
细胞实验
Apoptosis, TNF, Ferroptosis, Influenza Virus, Reactive Oxygen Species, ROS, Endogenous Metabolite
