Cytotoxic effects of differentiated PC12 cell infected by prion protein 106-126 peptide
10.3760/cma.j.issn.1008-1372.2011.07.002
- VernacularTitle:朊蛋白106-126肽段在Prion病细胞模型中的作用机制研究
- Author:
Dongwei ZHANG
;
Shanji NAN
;
Jiexu ZHAO
- Publication Type:Journal Article
- Keywords:
PrPC proteins/TO;
Prion diseases/PA;
Apoptosis;
Oxidative stress;
Energy metabolism
- From:
Journal of Chinese Physician
2011;13(7):869-872
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the cytotoxic effects of differentiated PC12 cells afterinfected by prion protein 106-126 peptide.Methods The PC12 cells were infected by prion protein 106-126peptide after differentiated by nerve growthfactor(NGF).Cell viability andthe morphological changes were observed.The energy metabolize and apoptosis was detected.Results Afterinfected by this peptide,cell viability decreasedfrom(98.1±1.9)% to (69.2±4.7)%,and apoptosis peak Was observed byflow cytometry.Aboutthe process of the cytotoxic effects,afterthe cells affected by PrP106-126,oxidative stress presented and existed continually,and then the intracellular free calcium concentrate increased from (185.74±12.93)nmol/L to (493.00±58.71)nmol/L subsequently,the activity of Ca2+ ATPase decreased from 54.92±4.05 to 34.92±4.86,the mitochondrial membrane potential decreasedto 65%,and also the energy metabolize disorder,the cells presented apoptosisinthe end.The changed Bcl-2/Bax system involvedinthe apoptosis.Conclusions Prion protein106-126 peptide caninduce apoptosisin differentiated PC12 cells and presented cellulartoxicity definitely.It might be a perfect model to study the cellular toxicity of prion protein.Continual oxidative stress could causetheintracellularfree calcium concentrate and disturb the energy metabolize,and the apoptosis might be the end-result.The oxidative stress of might play a startup and important role.
