摘要
目的:探讨TAT-tCNTF、TAT48-58、rhCNTF对Aβ损伤/非损伤SH-SY5Y细胞模型的GSH水平和SOD酶活性的影响,以分别评价其抗氧化应激效应。方法:采用析因设计研究经TAT-tCNTF、TAT48-58和rhCNTF处理后,Aβ损伤/不损伤的SH-SY5Y细胞模型的GSH水平和SOD酶活性;采用单因素多水平设计五个浓度水平的TAT48-58对SH-SY5Y细胞的GSH水平和SOD酶活性。结果:不同蛋白类型对GSH水平和SOD活性影响的结果分别为F=11.13,P<0.000 1和F=10.18,P<0.000 1。TAT-tCNTF与SH-SY5Y共孵育后损伤和非损伤模型的SOD活性和GSH水平分别为(0.57±0.01)%,(0.61±0.02)%和(5283±578)U.L-1,(6394±173)U.L-1。加入不同TAT48-58浓度对SH-SY5Y细胞的SOD活性和GSH含量影响方差分析FSOD=1.86,P=0.156 6,FGSH=1.55,P=0.261 7。结论:TAT-tCNTF能提高Aβ损伤的SH-SY5Y细胞模型的GSH水平和SOD活性的效应,TAT48-58不能引起细胞内氧化应激作用。
Objective： To investigate the effects on GSH levels and SOD activities of TAT-tCNTF, TAT48-58 and rhCNTF in Aft injured/uninjured SH-SY5Y cell model to evaluate the anti-oxidative stress ability respectively. Methods： The factorial design was used to investigate the effects on GSH levels and SOD activities of damaged/undamaged SH-SY5Y cells incubated with TAT- tCNTF, TAT48-58 and rhCNTF. And single-factor, multi-level design was used to investigate the effects on GSH levels and SOD activities of SH-SY5Y cells incubated with five different levels of concentration. Results： The results of GSH level and SOD activities affected by different kinds of protein were F = 11.13, P 〈 0.000 1 and F = 10.18, P 〈 0.000 1. The SOD activities of the SH-SY5Y damaged and undamaged model treated with TAT-tCNTF were （0.57± 0.01）% and （0.61 ± 0.02）% and GSH levels were （5283± 578） U·L^-1, （6394 ± 173）U·L^-1. The analysis of variance results to the activity ratio of SOD and concentration of GSH in SH- SY5Ycells after being treated by concentrations of TAT48-58 were FSOD = 1.86, P = 0.156 6, FGSH = 1.55, P = 0.261 7. Conclusion： TAT-tCNTF has the ability to improve the level of GSH and SOD in SH-SY5Y cell models damaged by Aft and TAT48_58 has nothing to do with the anti-oxidative stress ability.
出处
《中国药物应用与监测》
CAS
2012年第5期256-261,共6页
Chinese Journal of Drug Application and Monitoring
基金
国家自然科学基金青年科学基金项目(81001438)
关键词
阿尔茨海默病
睫状神经营养因子
反义激活转录蛋白
蛋白转导域
析因设计
氧化应激
Alzheimer disease
Ciliary neurotrophic factor
Antisense transcription protein
Protein transduction domain
Factorial design
Oxidative stress
