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Journal of the Korean Neurological Association 2014;32(2): 72-81.
3,4,5-Tricaffeoylquinic acid가 파킨슨증후군 유발독소 1-methyl-4-phenylpyridinium에 의한 세포자멸사에 미치는 억제효과
주재정, 강진호 한정호 김두응 이정수
중앙보훈병원 신경과, 중앙대학교 의과대학 약리학교실 a
Inhibitory Effect of 3,4,5-Tricaffeoylquinic Acid on Parkinsonian Toxin 1-Methyl-4-phenylpyridinium-induced Apoptosis
Jae-Jeong Joo
Department of Neurology, VHS Medical Center, Seoul, Korea Department of Pharmacology a , Chung-Ang University College of Medicine, Seoul, Korea
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. Key Words: 3,4,5-Tricaffeoylquinic acid, 1-Methyl-4-phenylpyridinium, PC12 cells, Apoptosis-related proteins, Protection