These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: 15-Deoxy-delta12,14-prostaglandin J2, a neuroprotectant or a neurotoxicant?
    Author: Koh SH, Jung B, Song CW, Kim Y, Kim YS, Kim SH.
    Journal: Toxicology; 2005 Dec 15; 216(2-3):232-43. PubMed ID: 16191461.
    Abstract:
    15-Deoxy-delta12,14-prostaglandin J2 (15d-PGJ2) is a potent ligand for peroxisome proliferators-activated receptor gamma (PPARgamma). However, its various effects independent of PPARgamma have recently been observed. The effect of 15d-PGJ2 on neuronal cells is still controversial. We investigated its effect on neuronal cells (N18D3 cells). When N18D3 cells were treated with 15d-PGJ2, the viability was not changed up to 8 microM, but decreased at higher than 8 microM. The expressions of survival signals, such as p85a phosphatidylinositol 3-kinase, phospho-Akt, and phospho-glycogen synthase kinase-3 beta (Ser-9), slightly increased up to 8 microM, however, decreased at higher than 8 microM. The levels of free radicals and membrane lipid peroxidation and the expression of c-Jun N-terminal Kinase increased in a dose-dependent manner, especially at higher than 8 microM. However, the expressions of death signals, such as cytosolic cytochrome c, activated caspase-3, and cleaved poly(ADP-ribose) polymerase, decreased up to 8 microM, however, increased at higher than 8 microM. In the study to evaluate whether low dose of 15d-PGJ2, up to 8 microM, had protective effect on oxidative stress-injured N18D3 cells, compared to the cells treated with only 100 microM H2O2, the pretreatment with 8 microM 15d-PGJ2 increased the viability and the expressions of the survival signals, but decreased them of the death signals. These results indicate that 15d-PGJ2 could be a neuroprotectant or a neurotoxicant, depending on its concentration. Therefore, some specific optimum dose of 15d-PGJ2 may be a new potential therapeutic candidate for oxidative stress-injury model of neurodegenerative diseases.
    [Abstract] [Full Text] [Related] [New Search]