Celecoxib, indomethacin and ibuprofen prevent 6-hydroxydopamine-induced PC12 cell death through the inhibition of NFκB and SAPK/JNK pathways | ||
| Iranian Journal of Basic Medical Sciences | ||
| مقاله 3، دوره 22، شماره 5، مرداد 2019، صفحه 477-484 اصل مقاله (1.05 M) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2019.34011.8091 | ||
| نویسندگان | ||
| Elham Ramazani1؛ Zahra Tayarani-Najaran2، 3؛ Masoud Fereidoni* 1 | ||
| 1Department of Biology, Faculty of Science, Ferdowsi University of Mashhad, Mashhad, Iran | ||
| 2Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran | ||
| 3Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran | ||
| چکیده | ||
| Objective(s): The possible action of nonsteroidal anti-inflammatory drugs (NSAIDs) in the reduction of reactive oxygen species (ROS) and also as anti-apoptotic agents may suggest them as putative agents for the treatment of neurodegenerative diseases. This study was designed to explore some pathways alterations induced by NSAIDs following 6-hydroxydopamine (6-OHDA)-induced cell death in PC12 cells as an in vitro model of Parkinson's disease (PD) and to compare the effects of celecoxib, indomethacin and ibuprofen. Materials and Methods: The cell viability, ROS content, glutathione (GSH) level, and apoptosis were measured using resazurin, dichlorofluorescein diacetate (DCFH-DA), 5,5′-dithiobis-2-nitrobenzoic acid (DTNB), propidium iodide (PI) and flowcytometry, real-time PCR and western blot. Results: Based on the results, pretreatment with celecoxib, indomethacin and ibuprofen for 24 hr significantly induced concentration and time-dependent protection against 6-OHDA-induced PC12 cell death. Cell viability (P<0.001), GSH level (P<0.01) and cytoplasmic content of nuclear factor kappa B (NFκB) (P<0.01) were increased, also ROS content (P<0.001) and apoptosis biomarkers such as the cleaved caspase-3 (P<0.001), Bax (P<0.01), phospho- stress-activated protein kinases / c-Jun N-terminal kinases (P-SPAK/JNK) (P<0.01) and cleaved poly ADP ribose polymerase (PARP) (P<0.001) protein levels were all decreased after pretreatment of cells with NSAIDs in 6-OHDA-induced PC12 cells. Conclusion: It is suggested that NFκB and SAPK/JNK pathways have an important role in 6-OHDA-induced cell injury. Overall, it seems that pretreatment with NSAIDs protect dopaminergic cells and may have the potential to slow the progression of PD. | ||
| کلیدواژهها | ||
| Apoptosis؛ Glutathione؛ NSAIDs؛ Parkinson's disease؛ PC12 Cells؛ ROS | ||
| مراجع | ||
|
1. Jankovic J. Parkinson’s disease: clinical features and diagnosis. J Neurol Neurosurg Psychiatry 2008; 79: 368-76. 2. Abeliovich A, Flint Beal M. Parkinsonism genes: culprits and clues. J Neurochem 2006; 99: 1062-72. 3. Winklhofer KF, Haass C. Mitochondrial dysfunction in Parkinson’s disease. Biochim Biophys Acta 2010; 1802: 29-44. 4. Ajmone-Cat MA, Bernardo A, Greco A, Minghetti L. Non-steroidal anti-inflammatory drugs and brain inflammation: effects on microglial functions. Pharmaceuticals 2010; 3: 1949-65. 5. Rouzer CA, Lawrence JM. Cyclooxygenases: structural and functional insights. J Lipid Res 2009; 50: S29-S34. 6. Warner TD, Giuliano F, Vojnovic I, Bukasa A, Mitchell JA, Vane JR. Nonsteroid drug selectivities for cyclooxygenase- 1 rather than cyclo-oxygenase-2 are associated with human gastrointestinal toxicity: a full in vitro analysis. Proc Natl Acad Sci U S A 1999; 96: 7563-7568. 7. G Perrone M, Scilimati A, Simone L, Vitale P. Selective COX-1 inhibition: A therapeutic target to be reconsidered. Curr Med Chem 2010; 17:3769-3805. 8. Zhang B, Shen Q, Chen Y, Pan R, Kuang S, Liu G, et al. Myricitrin alleviates oxidative stress-induced inflammation and apoptosis and protects mice against diabetic cardiomyopathy. Sci Rep 2017; 7: 44239-44255. 9. Mahmood KAS, Ahmed JH, Jawad AM. Non-steroidal anti-inflammatory drugs (NSAIDs), free radicals and reactive oxygen species (ros): a review of literature. Med J Basrah Univ 2009; 27: 46-53. 10. Laube M, Kniess T, Pietzsch J. Development of antioxidant COX-2 inhibitors as radioprotective agents for radiation therapy—a hypothesis-driven review. Antioxidants 2016; 5: 14-44. 11. Haghdoost-Yazdi H, Sarookhani M, Faraj A, Fraidouni N, Dargahi T, Yaghoubidoust MH, et al. Evaluation of the association between blood homocysteine concentration and the degree of behavioral symptoms in the 6-hydroxydopamine-induced Parkinsonism in rat. Pharmacol Biochem Behav 2014; 124: 297-304. 12. Ryu EJ, Angelastro JM, Greene LA. Analysis of gene expression changes in a cellular model of Parkinson disease. Neurobiol Dis 2005; 18: 54-74. 13. Samii A, Etminan M, Wiens MO, Jafari S. NSAID use and the risk of Parkinson’s disease: systematic review and meta-analysis of observational studies. Drugs Aging 2009; 26:769-79. 14. Gao X, Chen H, Schwarzschild MA, Ascherio A. Use of ibuprofen and risk of Parkinson disease. Neurology 2011; 76: 863-869. 15. Mousavi SH, Motaez M, Zamiri-Akhlaghi A, Emami SA, Tayarani-Najaran Z. In-Vitro evaluation of cytotoxic and apoptogenic properties of Sophora Pachycarpa. Iran. J Pharm Res 2014; 13: 665-673. 16. O’brien J, Wilson I, Orton T, Pognan F. Investigation of the Alamar Blue (resazurin) fluorescent dye for the assessment of mammalian cell cytotoxicity. Eur J Biochem 2000; 267: 5421-5426. 17. Tayarani-Najaran Z, Sareban M, Gholami A, Emami SA, Mojarrab M. Cytotoxic and apoptotic effects of different extracts of Artemisia turanica Krasch on K562 and HL-60 cell lines. Sci World 2013; 2013: 628073-628078. 18. Chen X, Zhong Z, Xu Z, Chen L, Wang Y. 2′, 7′-Dichlorodihydrofluorescein as a fluorescent probe for reactive oxygen species measurement: forty years of application and controversy. Free Radic Res 2010; 44: 587-604. 19. Lin CM, Lin RD, Chen ST, Lin YP, Chiu WT, Lin JW, et al. Neurocytoprotective effects of the bioactive constituents of Pueraria thomsonii in 6-hydroxydopamine (6-OHDA)- treated nerve growth factor (NGF)-differentiated PC12 cells. Phytochemistry 2010; 71: 2147-56. 20. Paglia DE, Valentine WN. Studies on the quantitative and qualitative characterization of erythrocyte glutathione peroxidase. J Lab Clin Med 1967; 70: 158-69. 21. Riccardi C, Nicoletti I. Analysis of apoptosis by propidium iodide staining and flow cytometry. Nat Protoc 2006; 1: 1458. 22. Hosseinzadeh L, Behravan J, Mosaffa F, Bahrami G, Bahrami A, Karimi G. Curcumin potentiates doxorubicin-induced apoptosis in H9c2 cardiac muscle cells through generation of reactive oxygen species. Food Chem Toxicol 2011; 49: 1102-9. 23. Anushre E, Aravind P, Thimappa GS, Devaraju KS. Parkinson’s disease genes expression study by QPCR in nitrosative stress induced pc12 cell line. Int J Pharm Bio Sci 2017; 8: 49-56. 24. Perumal AS, Tordzro WK, Katz M, Jackson-Lewis V, Cooper TB, Fahn S, et al. Regional effects of 6-hydroxydopamine (6-OHDA) on free radical scavengers in rat brain. Brain Res 1989; 504: 139-141. 25. Blum D, Torch S, Lambeng N, Nissou MF, Benabid AL, Sadoul R, et al. Molecular pathways involved in the neurotoxicity of 6-OHDA, dopamine and MPTP: contribution to the apoptotic theory in Parkinson’s disease. Prog Neurobiol 2001; 65: 135-172. 26. Gupta A, Kumar A, Kulkarni SK. Targeting oxidative stress, mitochondrial dysfunction and neuroinflammatory signaling by selective cyclooxygenase (COX)-2 inhibitors mitigates MPTP-induced neurotoxicity in mice. Prog Neuropsychopharmacol Biol Psychiatry 2011; 35: 974-981. 27. Tasaki Y, Yamamoto J, Omura T, Sakaguchi T, Kimura N, Ohtaki KI, et al. Meloxicam ameliorates motor dysfunction and dopaminergic neurodegeneration by maintaining Akt-signaling in a mouse Parkinson’s disease model. Neurosci Lett 2012; 521: 15-19. 28. Moore AH, Bigbee MJ, Boynton GE, Wakeham CM, Rosenheim HM, Staral CJ, et al. Non-steroidal Anti-inflammatory drugs in alzheimer’s disease and parkinson’s disease: Reconsidering the role of neuroinflammation. Pharmaceuticals 2010; 3: 1812-1841. 29. Świątkiewicz M, Zaremba M, Joniec I, Cz³onkowski A, Kurkowska-Jastrzêbska I. Potential neuroprotective effect of ibuprofen, insights from the mice model of Parkinson’s. Pharmacol Rep 2013; 65: 1227-1236. 30. Končič M, Rajič Z, Petrič N, Zorc B. Antioxidant activity of NSAID hydroxamic acids. Acta Pharm 2009; 59: 235-242. 31. Bassani TB, Vital MA, Rauh LK. Neuroinflammation in the pathophysiology of Parkinson’s disease and therapeutic evidence of anti-inflammatory drugs. Arq Neuropsiquiatr 2015; 73: 616-623. 32. Asanuma M, Miyazaki I. Nonsteroidal anti-inflammatory drugs in experimental parkinsonian models and Parkinson’s disease. Curr Pharm Des 2008; 14: 1428-1434. 33. Lee M, McGeer E, Kodela R, Kashfi K, McGeer PL. NOSH‐aspirin (NBS‐1120), a novel nitric oxide and hydrogen sulfide releasing hybrid, attenuates neuroinflammation induced by microglial and astrocytic activation: A new candidate for treatment of neurodegenerative disorders. Glia 2013; 61: 1724-1734. 34. Chinery R, Beauchamp RD, Shyr Y, Kirkland SC, Coffey RJ, Morrow JD. Antioxidants reduce cyclooxygenase-2 expression, prostaglandin production, and proliferation in colorectal cancer cells. Cancer Res 1998; 58: 2323-2327. 35. Łanocha-Arendarczyk N, Baranowska-Bosiacka I, Kot K, Gutowska I, Kolasa-Wołosiuk A, Chlubek D, et al. Expression and activity of COX-1 and COX-2 in Acanthamoeba sp.-infected lungs according to the host immunological statusInt. J Mol Sci 2018; 19: 121-138. 36. Suzuki Y, Inoue T, Ra C. NSAIDs, mitochondria and calcium signaling: special focus on aspirin/salicylates. Pharmaceuticals 2010; 3: 1594-1613. | ||
|
آمار تعداد مشاهده مقاله: 1,209 تعداد دریافت فایل اصل مقاله: 950 |
||