Cytoprotective Effect of 15-deoxy-Delta(12,14) Prostaglandin J2 (15d-PGJ2) against H2O2 Induced Death of Neuronally-differentiated PC12 Cells.
- Author:
Dong Ho OH
1
;
Seong Ho KOH
;
Boo CHUNG
;
Kee Hyung PARK
;
Hyun Young KIM
;
Chi Won SONG
;
Youngchul KIM
;
Juhan KIM
;
Myung Ho KIM
;
Seung Hyun KIM
Author Information
1. Department of Neurology, College of Medicine, Hanyang University, Seoul, Korea. kimsh1@hanyang.ac.kr
- Publication Type:Original Article
- Keywords:
Apoptosis;
Neurodegenerative disease;
Antioxidants;
Cytochrome c;
Caspase-3
- MeSH:
Animals;
Antioxidants;
Apoptosis;
Blotting, Western;
Caspase 3;
Cell Survival;
Cytochromes c;
Models, Theoretical;
Neurodegenerative Diseases;
Oxidative Stress;
PC12 Cells*
- From:Journal of the Korean Neurological Association
2006;24(1):58-65
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Neurodegenerative diseases are associated with oxidative stress. Antioxidants including 15-deoxy- Delta (12,14) prostaglandin J2 (15d-PGJ2) have been tried as potential therapeutic regimens of the experimental model of neurodegenerative disease. In this study, we investigated the neuroprotective role of 15d-PGJ2 on cytochrome c mediated apoptotic signals in oxidative stress injured neuronally-differentiated PC12 cells (nPC12 cells) by exposing them to H2O2. METHODS: Following 100 micor M H2O2 exposure, the viability of nPC12 cells (pretreated with 15d-PGJ2 vs. not pretreated) was evaluated by using MTT assay. Immunoreactivity (IR) of cytochrome c, caspase-3, and poly (ADP-ribose) polymerase (PARP) was examined by using a Western blot. RESULTS: In this study, 15d-PGJ2 pretreated nPC12 cells showed an increase in cell viability until the concentrations of 15d-PGJ2 reached up to 4 micor M, but there was no increment of cell viability in higher concentrations. The inhibition of cytochrome c release, activation of caspase-3, and cleavage of PARP were demonstrated by the pretreatment of 15d-PGJ2 up to 4 micor M. However, these were not observed in the pretreatment with 8 micor M 15d-PGJ2. CONCLUSIONS: These data show that 15d-PGJ2 affects the apoptotic pathway through downstream signals including cytochrome c and caspase-3 pathway. Therefore, these results suggest that 15d-PGJ2 could be a new potential therapeutic candidate for the oxidative stress-injury model of neurodegenerative diseases.
