| 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 |
|
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|
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| 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 |
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