3,4,5-Tricaffeoylquinic acid가 파킨슨증후군유발독소 1-methyl-4-phenylpyridinium에 의한세포자멸사에 미치는 억제효과
Inhibitory Effect of 3,4,5-Tricaffeoylquinic Acid on Parkinsonian Toxin 1-Methyl-4-phenylpyridinium-induced Apoptosis
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Background: 1-Methyl-4-phenylpyridinium (MPP) causes a neuronal cell injury that is similar to the findings observedin 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 ofparkinsonian toxin MPP+remains unclear. Methods: Using differentiated PC12 cells, the preventive effect of 3,4,5-triCQA on the MPP+-induced cell death inrelation 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 mitochondrialtransmembrane potential, cytochrome c release, activation of caspases (-8, -9 and -3), cleavage of PARP-1, and an increasein the tumor suppressor p53 levels. 3,4,5-Tricaffeoylquinic acid attenuated the MPP+-induced changes in theapoptosis-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 theactivation of the mitochondrial pathway and the caspase-8- and Bid-dependent pathways. The preventive effect seems tobe ascribed to its inhibitory effect on the formation of reactive oxygen species and depletion of GSH.
Abstract
Background: 1-Methyl-4-phenylpyridinium (MPP+) causes a neuronal cell injury that is similar to the findings observedin 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 ofparkinsonian toxin MPP+remains unclear. Methods: Using differentiated PC12 cells, the preventive effect of 3,4,5-triCQA on the MPP+-induced cell death inrelation 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 mitochondrialtransmembrane potential, cytochrome c release, activation of caspases (-8, -9 and -3), cleavage of PARP-1, and an increasein the tumor suppressor p53 levels. 3,4,5-Tricaffeoylquinic acid attenuated the MPP+-induced changes in theapoptosis-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 theactivation of the mitochondrial pathway and the caspase-8- and Bid-dependent pathways. The preventive effect seems tobe ascribed to its inhibitory effect on the formation of reactive oxygen species and depletion of GSH.
참고문헌 (32)
- Schapira AH, "Etiology and pathogenesis of Parkinson's disease", Mov Disord, 26, pp.1049~1055 (2011)
- Przedborski S, "The parkinsonian toxin MPTP: action and mechanism", Restor Neurol Neurosci, 16, pp.135~142 (2000)
- Chuenkova MV, "PDNF, a human parasite-derived mimic of neurotrophic factors, prevents caspase activation, free radical formation, and death of dopaminergic cells exposed to the Parkinsonisminducing neurotoxin MPP+", Brain Res Mol Brain Res, 119, pp.50~61 (2003)
- Jenner P, "Oxidative stress in Parkinson’s disease", Ann Neurol, 53, pp.S26~S38 (2003)
- Ott M, "Mitochondria, oxidative stress and cell death", Apoptosis, 12, pp.913~922 (2007)
- Storch A, "Dopamine transporter: involvement in selective dopaminergic neurotoxicity and degeneration", J Neural Transm, 111, pp.1267~1286 (2004)
- Lee CS, "Modulation of 1-methyl-4-phenylpyridinium-induced mitochondrial dysfunction and cell death by KATP channel block", J Neural Transm, 114, pp.297~305 (2007)
- Viswanath V, "Caspase-9 activation results in downstream caspase-8 activation and bid cleavage in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridineinduced Parkinson's disease", J Neurosci, 21, pp.9519~9528 (2001)
- Geng X, "Neuroprotective effects of echinacoside in the mouse MPTP model of Parkinson's disease", Eur J Pharmacol, 564, pp.66~74 (2007)
- Kim SS, "Neuroprotective effects of 3,5-dicaffeoylquinic acid on hydrogen peroxide-induced cell death in SH-SY5Y cells", Phytother Res, 19, pp.243~245 (2005)
- Park KH, "The anti-oxidative and anti-inflammatory effects of caffeoyl derivatives from the roots of Aconitum koreanum R. RAYMOND", Biol Pham Bull, 32, pp.2029~2033 (2009)
- dos Santos MD, "Effects of caffeoylquinic acid derivatives and C-flavonoid from Lychnophora ericoides on in vitro inflammatory mediator production", Nat Prod Commun, 5, pp.733~740 (2010)
- Lee CS, "3,4,5-Tricaffeoylquinic acid inhibits tumor necrosis factor-α-stimulated production of inflammatory mediators in keratinocytes via suppression of Akt- and NF-κB-pathways", Int Immunopharmacol, 11, pp.1715~1723 (2011)
- Bonuccelli U, "New pharmacological horizons in the treatment of Parkinson disease", Neurology, 67, pp.S30~S38 (2006)
- Lipman T, "Neuroprotective effects of the stable nitroxide compound Tempol on 1-methyl-4-phenylpyridinium ion-induced neurotoxicity in the nerve growth factor-differentiated model of pheochromocytoma PC12 cells", Eur J Pharmacol, 549, pp.50~57 (2006)
- Wu Y, "Protective effect of erythropoietin against 1-methyl-4-phenylpyridinium-induced neurodegenaration in PC12 cells", Neurosci Bull, 23, pp.156~164 (2007)
- Tatton WG, "Propargylamines induce antiapoptotic new protein synthesis in serum-and nerve growth factor (NGF)-withdrawn, NGF-differentiated PC-12 cells", J Pharmacol Exp Ther, 301, pp.753~764 (2002)
- Mosmann T, "Rapid colorimetric assay for cellular growth and survival:application to proliferation and cytotoxicity assays", J Immunol Methods, 65, pp.55~63 (1983)
- Andrisano V, "Studies on the photostability and in vitro phototoxicity of Labetalol", Eur J Pharm Sci, 12, pp.495~504 (2001)
- Berthier A, "Involvement of a calcium-dependent dephosphorylation of BAD associated with the localization of Trpc-1 within lipid rafts in 7-ketocholesterol-induced THP-1 cell apoptosis", Cell Death Differ, 11, pp.897~905 (2004)
- Fu W, "Catecholamines potentiate amyloid β-peptide neurotoxicity: involvement of oxidative stress, mitochondrial dysfunction, and perturbed calcium homeostasis", Neurobiol Dis, 5, pp.229~243 (1998)
- van Klaveren RJ, "Increase in γ-glutamyltransferase by glutathione depletion in rat type II pneumocytes", Free Radic Biol Med, 22, pp.525~534 (1997)
- Camins A, "Apoptotic mechanisms involved in neurodegenerative diseases: experimental and therapeutic approaches", Methods Find Exp Clin Pharmacol, 30, pp.43~65 (2008)
- Hu W, "Anticancer therapy targeting the apoptotic pathway", Lancet Oncol, 4, pp.721~729 (2003)
- Jin Z, "Overview of cell death signaling pathways", Cancer Biol Ther, 4, pp.139~163 (2005)
- Chipuk JE, "Dissecting p53-dependent apoptosis", Cell Death Differ, 13, pp.994~1002 (2006)
- Chen F, "Current strategies to target p53 in cancer", Biochem Pharmacol, 80, pp.724~730 (2010)
- Armstrong JS, "Mitochondria: a target for cancer therapy", Br J Pharmacol, 147, pp.239~248 (2006)
- Mignotte B, "Mitochondria and apoptosis", Eur J Biochem, 252, pp.1~15 (1998)
- Franco R, "Apoptosis and glutathione: beyond an antioxidant", Cell Death Differ, 16, pp.1303~1314 (2009)
- Franco R, "SLCO", OATP-like transport of glutathione in FasL-induced apoptosis: glutathione efflux is coupled to an organic anion exchange and is necessary for the progression of the execution phase of apoptosis, 2006, pp.281, 29542~29557
- Circu ML, "Glutathione and apoptosis", Free Radic Res, 42, pp.689~706 (2008)