中国药理学通报
中國藥理學通報
중국약이학통보
Chinese Pharmacological Bulletin
2015年
11期
1505-1509
,共5页
N-乙酰基半胱氨酸%Aβ25-35%calpain%H2 O2%线粒体膜电位%ATP
N-乙酰基半胱氨痠%Aβ25-35%calpain%H2 O2%線粒體膜電位%ATP
N-을선기반광안산%Aβ25-35%calpain%H2 O2%선립체막전위%ATP
N-acetyl-L-cysteine%Aβ25-35%calpain%H2 O2%mitochondrial membrane potential%ATP
目的探讨 N-乙酰基半胱氨酸( N-acetyl-L-cysteine, NAC)对β淀粉样蛋白毒性片段25-35( Aβ25-35)活化cal-pain活性的影响及可能机制。方法运用Aβ25-35来诱导皮质神经元的损伤,实验分为空白对照组、Aβ25-35组、NAC与Aβ25-35共同作用组,采用荧光酶标法检测calpain活性、氧自由基( H2 O2)和线粒体膜电位；用化学发光法测定神经元内ATP水平。结果 Aβ25-35(20μmol·L-1)作用12 h可明显升高calpain活性；与 Aβ25-35处理组相比, NAC (10 mmol · L-1)预先作用24 h,然后再与Aβ25-35共同作用12 h,可明显降低 calpain活性；与空白对照组相比, Aβ25-35处理组中的H2 O2明显升高、线粒体膜电位和ATP水平明显下降；而与Aβ25-35处理组相比,NAC预处理组中的H2 O2水平下降、线粒体膜电位和ATP水平升高,这些差异皆有统计学意义。结论这些研究结果提示, NAC可能通过线粒体的保护作用来降低Aβ25-35诱导的异常活化的calpain活性。
目的探討 N-乙酰基半胱氨痠( N-acetyl-L-cysteine, NAC)對β澱粉樣蛋白毒性片段25-35( Aβ25-35)活化cal-pain活性的影響及可能機製。方法運用Aβ25-35來誘導皮質神經元的損傷,實驗分為空白對照組、Aβ25-35組、NAC與Aβ25-35共同作用組,採用熒光酶標法檢測calpain活性、氧自由基( H2 O2)和線粒體膜電位；用化學髮光法測定神經元內ATP水平。結果 Aβ25-35(20μmol·L-1)作用12 h可明顯升高calpain活性；與 Aβ25-35處理組相比, NAC (10 mmol · L-1)預先作用24 h,然後再與Aβ25-35共同作用12 h,可明顯降低 calpain活性；與空白對照組相比, Aβ25-35處理組中的H2 O2明顯升高、線粒體膜電位和ATP水平明顯下降；而與Aβ25-35處理組相比,NAC預處理組中的H2 O2水平下降、線粒體膜電位和ATP水平升高,這些差異皆有統計學意義。結論這些研究結果提示, NAC可能通過線粒體的保護作用來降低Aβ25-35誘導的異常活化的calpain活性。
목적탐토 N-을선기반광안산( N-acetyl-L-cysteine, NAC)대β정분양단백독성편단25-35( Aβ25-35)활화cal-pain활성적영향급가능궤제。방법운용Aβ25-35래유도피질신경원적손상,실험분위공백대조조、Aβ25-35조、NAC여Aβ25-35공동작용조,채용형광매표법검측calpain활성、양자유기( H2 O2)화선립체막전위；용화학발광법측정신경원내ATP수평。결과 Aβ25-35(20μmol·L-1)작용12 h가명현승고calpain활성；여 Aβ25-35처리조상비, NAC (10 mmol · L-1)예선작용24 h,연후재여Aβ25-35공동작용12 h,가명현강저 calpain활성；여공백대조조상비, Aβ25-35처리조중적H2 O2명현승고、선립체막전위화ATP수평명현하강；이여Aβ25-35처리조상비,NAC예처리조중적H2 O2수평하강、선립체막전위화ATP수평승고,저사차이개유통계학의의。결론저사연구결과제시, NAC가능통과선립체적보호작용래강저Aβ25-35유도적이상활화적calpain활성。
Aim To explore the effect of N-acetyl-L-cysteine ( NAC ) on β amyloid peptide 25 - 35 ( Aβ25-35 )-induced the increase of calpain activity and its possible mechanism. Methods The activity of cal-pain was induced by 20μmol·L-1 Aβ 25-35 in primary cortical neuron. Neurons were incubated in the absent or present Aβ25-35 , or pre-incubated NAC ( 10 mmol ·L-1 ) , then co-incubated with Aβ25-35 . The meas-urement of calpain activity, H2 O2 level and mitochon-drial membrane potential was performed on a micro-plate fluorometer. The ATP level was detected using a luciferin/luciferase based ATP assay kit. Results In Aβ25-35 treated group, the activity of calpain and H2 O2 was obviously higher than that in control group. How-ever, in neurons pre-incubated in NAC and then co-in-cubated in Aβ25-35 , the calpain activity and H2 O2 level were significantly decreased compared with that in Aβ25-35 group. Upon Aβ25-35 exposure for 12 h, corti-cal neurons showed a significant decrease in mitochon-drial membrane potential and ATP level when com-pared to the control group. Pre-treatment with NAC showed an increase in mitochondrial membrane poten-tial and ATP level as compared to neurons treated with Aβ25-35 alone for 12h. Conclusion This result sug-gests that NAC can attenuate calpain activity induced by Aβ25-35 through protecting mitochondria.
