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Epigallocatechin gallate attenuates L-DOPA-induced apoptosis in rat PC12 cells

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In this study, the protective effects of EGCG on L-3,4-dihydroxyphenylalanine (L-DOPA)-induced oxidative cell death in catecholaminergic PC12cells, the in vitro model of Parkinson’s disease, were investigated. Treatment with L-DOPA at concentrations higher than 150 μM caused cytotoxicity in PC12 cells, as determined using the 3-(4,5-dimetylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry detection. The apoptotic ratio was similar in cells treated with 100 μM EGCG plus 150 μM L-DOPA (5.02%) and the control (0.96%) (P > 0.05), and was lower than that of cells treated with L-DOPA only (32.24%, P < 0.05). The generation level of ROS (% of control) in cells treated with EGCG plus L-DOPA was lower than that in cells treated with L-DOPA only (123.90% vs 272.32%, P < 0.05). The optical density in production of TBARS in cells treated with L-DOPA only was higher than that in the control (0.27 ± 0.05 vs 0.08 ± 0.04, P < 0.05), and in cells treated with EGCG only (0.14 ± 0.02, P < 0.05), and EGCG plus L-DOPA (0.13 ± 0.02, P < 0.05). The intracellular level of GSH in cells treated with EGCG plus L-DOPA was higher than that in cells treated with L-DOPA only (233.25 ± 16.44 vs 119.23 ± 10.25, P < 0.05). These results suggest that EGCG protects against L-DOPA-induced oxidative apoptosis in PC12 cells, and might be a potent neuroprotective agent.

Abstract

In this study, the protective effects of EGCG on L-3,4-dihydroxyphenylalanine (L-DOPA)-induced oxidative cell death in catecholaminergic PC12cells, the in vitro model of Parkinson’s disease, were investigated. Treatment with L-DOPA at concentrations higher than 150 μM caused cytotoxicity in PC12 cells, as determined using the 3-(4,5-dimetylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry detection. The apoptotic ratio was similar in cells treated with 100 μM EGCG plus 150 μM L-DOPA (5.02%) and the control (0.96%) (P > 0.05), and was lower than that of cells treated with L-DOPA only (32.24%, P < 0.05). The generation level of ROS (% of control) in cells treated with EGCG plus L-DOPA was lower than that in cells treated with L-DOPA only (123.90% vs 272.32%, P < 0.05). The optical density in production of TBARS in cells treated with L-DOPA only was higher than that in the control (0.27 ± 0.05 vs 0.08 ± 0.04, P < 0.05), and in cells treated with EGCG only (0.14 ± 0.02, P < 0.05), and EGCG plus L-DOPA (0.13 ± 0.02, P < 0.05). The intracellular level of GSH in cells treated with EGCG plus L-DOPA was higher than that in cells treated with L-DOPA only (233.25 ± 16.44 vs 119.23 ± 10.25, P < 0.05). These results suggest that EGCG protects against L-DOPA-induced oxidative apoptosis in PC12 cells, and might be a potent neuroprotective agent.

참고문헌 (43)

  1. Agid Y, "Parkinson's disease: pathophysiology", Lancet, 337, pp.1321~1324 (1991)
  2. Lee JJ, "Aggravation of L-DOPA-induced neurotoxicity by tetrahydropapaveroline in PC12 cells", Biochem Pharmacol, 66, pp.1787~1795 (2003)
  3. Migheli R, "Enhancing effect of manganese on L-DOPA-induced apoptosis in PC12 cells: role of oxidative stress", J Neurochem, 73, pp.1155~1163 (1999)
  4. Spencer JP, "Superoxide-dependent depletion of reduced glutathione by L-DOPA and dopamine. Relevance to Parkinson's disease", Neuroreport, 6, pp.1480~1484 (1995)
  5. Hirsch EC, "Biochemistry of Parkinson's disease with special reference to the dopaminergic systems", Mol Neurobiol, 9, pp.135~142 (1994)
  6. Mizuno Y, "Role of mitochondria in the etiology and pathogenesis of Parkinson's disease", Biochim Biophys Acta, 1271, pp.265~274 (1995)
  7. Dexter DT, "Basal lipid peroxidation in substantia nigra is increased in Parkinson's disease", J Neurochem, 52, pp.381~389 (1989)
  8. Chung KK, "New insights into Parkinson's disease", J Neurol, 250(Suppl 3), pp.III15~III24 (2003)
  9. Heo HJ, "Effects of banana, orange, and apple on oxidative stress-induced neurotoxicity in PC12 cells", J Food Sci, 73, pp.H28~H32 (2008)
  10. Bastianetto S, "The Ginkgo biloba extract (EGb 761) protects and rescues hippocampal cells against nitric oxide-induced toxicity: involvement of its flavonoid constituents and protein kinase C", J Neurochem, 74, pp.2268~2277 (2000)
  11. Bordoni A, "Green tea protection of hypoxia", reoxygenation injury in cultured cardiac cells, 2002, pp.13, 103~111
  12. Nie G, "Distinct effects of tea catechins on 6-hydroxydopamine-induced apoptosis in PC12 cells", Arch Biochem Biophys, 397, pp.84~90 (2002)
  13. Song DU, "Effect of drinking green tea on ageassociated accumulation of Maillard-type fluorescence and carbonyl groups in rat aortic and skin collagen", Arch Biochem Biophys, 397, pp.424~429 (2002)
  14. Dong Z, "Inhibition of tumor promoterinduced activator protein 1 activation and cell transformation by tea polyphenols, (-)-epigallocatechin gallate, and theaflavins", Cancer Res, 57, pp.4414~4419 (1997)
  15. Guo Q, "Studies on protective mechanisms of four components of green tea polyphenols against lipid peroxidation in synaptosomes", Biochim Biophys Acta, 1304, pp.210~222 (1996)
  16. Guo Q, "ESR study on the structure-antioxidant activity relationship of tea catechins and their epimers", Biochim Biophys Acta, 1427, pp.13~23 (1999)
  17. Jin CF, "Different effects of five catechins on 6-hydroxydopamine-induced apoptosis in PC12 cells", J Agric Food Chem, 49, pp.6033~6038 (2001)
  18. Levites Y, "Attenuation of 6-hydroxydopamine (6-OHDA)-induced nuclear factor-kappaB (NF-kappaB) activation and cell death by tea extracts in neuronal cultures", Biochem Pharmacol, 63, pp.21~29 (2002)
  19. Yoneda T, "Antioxidant effects of "beta catechin"", Biochem Mol Biol Int, 35, pp.995~1008 (1995)
  20. Koh SH, "Epigallocatechin gallate protects nerve growth factor differentiated PC12 cells from oxidative-radical-stress-induced apoptosis through its effect on phosphoinositide 3-kinase", Akt and glycogen synthase kinase-3, 2003, pp.118, 72~81[DOI]
  21. Casarejos MJ, "Differential effects of L-DOPA on monoamine metabolism, cell survival and glutathione production in midbrain neuronal-enriched cultures from parkin knockout and wild-type mice", J Neurochem, 94, pp.1005~1014 (2005)
  22. Walkinshaw G, "Induction of apoptosis in catecholaminergic PC12 cells by L-DOPA. Implications for the treatment of Parkinson's disease", J Clin Invest, 95, pp.2458~2464 (1995)
  23. Boyce S, "Nigrostriatal damage is required for induction of dyskinesias by L-DOPA in squirrel monkeys", Clin Neuropharmacol, 13, pp.448~458 (1990)
  24. Cheng N, "Differential neurotoxicity induced by L-DOPA and dopamine in cultured striatal neurons", Brain Res, 743, pp.278~283 (1996)
  25. Basma AN, "L-DOPA cytotoxicity to PC12 cells in culture is via its autoxidation", J Neurochem, 64, pp.825~832 (1995)
  26. Greene LA, "Establishment of a noradrenergic clonal line of rat adrenal pheochromocytoma cells which respond to nerve growth factor", Proc Natl Acad Sci U S A, 73, pp.2424~2428 (1976)
  27. Mosmann T, "Rapid colorimetric assay for cellular growth and survival: application to proliferation and cytotoxicity assays", J Immunol Methods, 65, pp.55~63 (1983)
  28. Gunasekar PG, "NMDA receptor activation produces concurrent generation of nitric oxide and reactive oxygen species: implication for cell death", J Neurochem, 65, pp.2016~2021 (1995)
  29. Draper HH, "Malondialdehyde determination as index of lipid peroxidation", Methods Enzymol, 186, pp.421~431 (1990)
  30. Griffith OW, "Determination of glutathione and glutathione disulfide using glutathione reductase and 2-vinylpyridine", Anal Biochem, 106, pp.207~212 (1980)
  31. Raza H, "In vitro effects of tea polyphenols on redox metabolism, oxidative stress, and apoptosis in PC12 cells", Ann N Y Acad Sci, 1138, pp.358~365 (2008)
  32. Watanabe H, "Alterations of human erythrocyte membrane fluidity by oxygen-derived free radicals and calcium", Free Radic Biol Med, 8, pp.507~514 (1990)
  33. Zeevalk GD, "Energy stress-induced dopamine loss in glutathione peroxidase-overexpressing transgenic mice and in glutathionedepleted mesencephalic cultures", J Neurochem, 68, pp.426~429 (1997)
  34. Levites Y, "Green tea polyphenol (-)-epigallocatechin-3-gallate prevents N-methyl- 4-phenyl-1,2,3,6-tetrahydropyridine-induced dopaminergic neurodegeneration", J Neurochem, 78, pp.1073~1082 (2001)
  35. Levites Y, "Attenuation of 6-hydroxydopamine (6-OHDA)-induced nuclear factor-kappaB (NF-kappaB) activation and cell death by tea extracts in neuronal cultures", Biochem Pharmacol, 63, pp.21~29 (2002)
  36. Levites Y, "Neuroprotection and neurorescue against Abeta toxicity and PKC-dependent release of nonamyloidogenic soluble precursor protein by green tea polyphenol (-)-epigallocatechin-3-gallate", FASEB J, 17, pp.952~954 (2003)
  37. Jeong JH, "Epigallocatechin 3-gallate attenuates neuronal damage induced by 3-hydroxykynurenine", Toxicology, 195, pp.53~60 (2004)
  38. 오원만, "Inhibition by epigallocatechin gallate of CoCl2-induced apoptosis in rat PC12 cells", LIFE SCIENCES, 80(15), pp.1355~1363 (2007), PERGAMON-ELSEVIER SCIENCE LTD
  39. Inanami O, "Oral administration of (-)catechin protects against ischemiareperfusion- induced neuronal death in the gerbil", Free Radic Res, 29, pp.359~365 (1998)
  40. Seyfried J, "Differential effects of L-buthionine sulfoximine and ethacrynic acid on glutathione levels and mitochondrial function in PC12 cells", Neurosci Lett, 264, pp.1~4 (1999)
  41. Wüllner U, "Glutathione depletion potentiates MPTP and MPP+ toxicity in nigral dopaminergic neurones", Neuroreport, 7, pp.921~923 (1996)
  42. Raza H, "Green tea polyphenol epigallocatechin-3-gallate differentially modulates oxidative stress in PC12 cell compartments", Toxicol Appl Pharmacol, 207, pp.212~220 (2005)
  43. Skrzydlewska E, "Protective effect of green tea against lipid peroxidation in the rat liver, blood serum and the brain", Phytomedicine, 9, pp.232~238 (2002)

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