Inhibitory Effect of 3,4,5-Tricaffeoylquinic Acid on Parkinsonian Toxin 1-Methyl-4-phenylpyridinium-induced Apoptosis.
- Author:
Jae Jeong JOO
1
;
Jin Ho KANG
;
Jeong Ho HAN
;
Doo Eung KIM
;
Chung Soo LEE
Author Information
1. Department of Neurology, VHS Medical Center, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
3,4,5-Tricaffeoylquinic acid;
1-Methyl-4-phenylpyridinium;
PC12 cells;
Apoptosis-related proteins;
Protection
- MeSH:
1-Methyl-4-phenylpyridinium;
Animals;
Apoptosis*;
Caspases;
Cell Death;
Cytochromes c;
Membrane Potentials;
Neurons;
Parkinson Disease;
PC12 Cells;
Reactive Oxygen Species
- From:Journal of the Korean Neurological Association
2014;32(2):72-81
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: 1-Methyl-4-phenylpyridinium (MPP+) causes a neuronal cell injury that is similar to the findings observed in Parkinson's disease. Caffeoylquinic acid derivatives have demonstrated anti-oxidant and anti-inflammatory effects. Nevertheless, the effect of 3,4,5-tricaffeoylquinic acid (3,4,5-triCQA) on the neuronal cell death due to exposure of parkinsonian toxin MPP+ remains unclear. METHODS: Using differentiated PC12 cells, the preventive effect of 3,4,5-triCQA on the MPP+-induced cell death in relation to apoptotic process was examined. RESULTS: MPP+ induced a decrease in Bid, Bcl-2 and survivin protein levels, increase in Bax levels, loss of the mitochondrial transmembrane potential, cytochrome c release, activation of caspases (-8, -9 and -3), cleavage of PARP-1, and an increase in the tumor suppressor p53 levels. 3,4,5-Tricaffeoylquinic acid attenuated the MPP+-induced changes in the apoptosis-related protein levels, formation of reactive oxygen species, depletion of GSH, nuclear damage and cell death. 3,4,5-Tricaffeoylquinic acid attenuated another parkinsonian neurotoxin rotenone-induced cell death. CONCLUSIONS: 3,4,5-Tricaffeoylquinic acid may attenuate the MPP+-induced apoptosis in PC12 cells by suppressing the activation of the mitochondrial pathway and the caspase-8- and Bid-dependent pathways. The preventive effect seems to be ascribed to its inhibitory effect on the formation of reactive oxygen species and depletion of GSH.
