Possible effect of N-acetyl-L-cysteine on Aβ25-35-induced increase of calpain activity
10.3969/j.issn.1001-1978.2015.11.007
- VernacularTitle:N-乙酰基半胱氨酸对Aβ25-35活化calpain活性的影响及可能机制
- Author:
Tianwen HUANG
;
Zhiying LIN
;
Xiaochun CHEN
- Publication Type:Journal Article
- Keywords:
N-acetyl-L-cysteine;
Aβ25-35;
calpain;
H2 O2;
mitochondrial membrane potential;
ATP
- From:
Chinese Pharmacological Bulletin
2015;(11):1505-1509
- CountryChina
- Language:Chinese
-
Abstract:
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.
