Implication of Caspase-3 as a Common Therapeutic Target for Multineurodegenerative Disorders and Its Inhibition Using Nonpeptidyl Natural Compounds

BioMed Research International

Volumn 2015, Issue , 2015, Pages

  Khan, Saif ^a   Ahmad, Khurshid ^b   Alshammari, Eyad M A ^a   Adnan, Mohd ^a   Baig, Mohd Hassan ^c   Lohani, Mohtashim ^b   Somvanshi, Pallavi ^d   Haque, Shafiul ^e,f  

^a UNIVERSITY OF HAIL   (Saudi Arabia)

^b INTEGRAL UNIVERSITY   (India)

^c Yeungnam University   (South Korea)

^d TERI UNIVERSITY   (India)

^e JAZAN UNIVERSITY   (Saudi Arabia)

^f JAMIA MILLIA ISLAMIA CENTRAL UNIVERSITY   (India)

Author keywords

[No Author keywords available]

Indexed keywords

APIGENIN; BERBERINE; BILOBALIDE; CASPASE 3; CHITOSAN; CURCUMIN; HUPERZINE A; LUTEOLIN; NATURAL PRODUCT; NONPEPTIDYL NATURAL COMPOUND; QUERCETIN; RESVERATROL; ROSMARINIC ACID; UNCLASSIFIED DRUG; CASPASE INHIBITOR; CINNAMIC ACID DERIVATIVE; DEPSIDE; LIGAND;

ARTICLE; BINDING AFFINITY; COMPUTER MODEL; DEGENERATIVE DISEASE; DRUG RECEPTOR BINDING; MOLECULAR DOCKING; PROTEIN INTERACTION; ALZHEIMER DISEASE; AMYOTROPHIC LATERAL SCLEROSIS; APOPTOSIS; CHEMISTRY; DRUG EFFECTS; HUMAN; HUNTINGTON DISEASE; NEURODEGENERATIVE DISEASES; PARKINSON DISEASE; PATHOLOGY;

ALZHEIMER DISEASE; AMYOTROPHIC LATERAL SCLEROSIS; APOPTOSIS; CASPASE 3; CASPASE INHIBITORS; CINNAMATES; CURCUMIN; DEPSIDES; HUMANS; HUNTINGTON DISEASE; LIGANDS; MOLECULAR DOCKING SIMULATION; NEURODEGENERATIVE DISEASES; PARKINSON DISEASE;

EID: 84929631283     PISSN: 23146133     EISSN: 23146141     Source Type: Journal    
DOI: 10.1155/2015/379817     Document Type: Article

References (46)

1. L. E. Hebert, L. A. Beckett, P. A. Scherr, and D. A. Evans, "Annual incidence of Alzheimer disease in the United States projected to the years 2000 through 2050," Alzheimer Disease and Associated Disorders, vol. 15, no. 4, pp. 169-173, 2001.
2. L. E. Hebert, P. A. Scherr, J. L. Bienias, D. A. Bennett, and D. A. Evans, "Alzheimer disease in the US population: prevalence estimates using the 2000 census," Archives of Neurology, vol. 60, no. 8, pp. 1119-1122, 2003.
3. I. Kanazawa, "How do neurons die in neurodegenerative diseases?"Trends in Molecular Medicine, vol. 7, no. 8, pp. 339-344, 2001.
4. A. G. Porterand R. U. Jänicke, "Emerging roles of caspase-3 in apoptosis," Cell Death & Differentiation, vol. 6, no. 2, pp. 99-104, 1999.
5. M. E. Nuttall, D. Lee, B. McLaughlin, and J. A. Erhardt, "Selective inhibitors of apoptotic caspases: implications for novel therapeutic strategies," Drug Discovery Today, vol. 6, no. 2, pp. 85-91, 2001.
6. M. G. Grütter, "Caspases: key players in programmed cell death," Current Opinion in Structural Biology, vol. 10, no. 6, pp. 649-655, 2000.
7. P. Fuentes-Prior and G. S. Salvesen, "The protein structures that shape caspase activity, specificity, activation and inhibition,"Biochemical Journal, vol. 384, no. 2, pp. 201-232, 2004.
8. A. Mohr and R. M. Zwacka, "In situ trapping of initiator caspases reveals intermediate surprises," Cell Biology International, vol. 31, no. 5, pp. 526-530, 2007.
9. A. Fleischer, A. Ghadiri, F. Dessauge et al., "Modulating apoptosis as a target for effective therapy," Molecular Immunology, vol. 43, no. 8, pp. 1065-1079, 2006.
10. R. C. Taylor, S. P. Cullen, and S. J. Martin, "Apoptosis: controlled demolition at the cellular level," Nature Reviews Molecular Cell Biology, vol. 9, no. 3, pp. 231-241, 2008.
11. C. A. Marques, U. Keil, A. Bonert et al., "Neurotoxic mechanisms caused by the alzheimer's disease-linked Swedish amyloid precursor protein. Mutation oxidative stress, caspases, and the JNK pathway," The Journal of Biological Chemistry, vol. 278, no. 30, pp. 28294-28302, 2003.
12. H. R. Stennicke and G. S. Salvesen, "Catalytic properties of the caspases," Cell Death and Differentiation, vol. 6, no. 11, pp. 1054-1059, 1999.
13. P. J. Lakshmi, B. V. S. Suneel Kumar, R. S. Nayana et al., "Design, synthesis, and discovery of novel non-peptide inhibitor of Caspase-3 using ligand based and structure based virtual screening approach," Bioorganic and Medicinal Chemistry, vol. 17, no. 16, pp. 6040-6047, 2009.
14. S. Sharma, A. Basu, and R. K. Agrawal, "Pharmacophore modeling and docking studies on some nonpeptide-based caspase-3 inhibitors," BioMed Research International, vol. 2013, Article ID 306081, 15 pages, 2013.
15. M. D'Amelio, M. Sheng, and F. Cecconi, "Caspase-3 in the central nervous system: beyond apoptosis," Trends in Neurosciences, vol. 35, no. 11, pp. 700-709, 2012.
16. N. Louneva, J. W. Cohen, L.-Y. Han et al., "Caspase-3 is enriched in postsynaptic densities and increased in Alzheimer's disease,"The American Journal of Pathology, vol. 173, no. 5, pp. 1488-1495, 2008.
17. L. J. Martin, A. C. Price, A. Kaiser, A. Y. Shaikh, and Z. Liu, "Mechanisms for neuronal degeneration in amyotrophic lateral sclerosis and in models of motor neuron death (review),"International Journal of Molecular Medicine, vol. 5, no. 1, pp. 3-13, 2000.
18. M. Li, V. O. Ona, C. Guégan et al., "Functional role of caspase-1 and caspase-3 in an ALS transgenic mouse model," Science, vol. 288, no. 5464, pp. 335-339, 2000.
19. W. Boston-Howes, S. L. Gibb, E. O. Williams, P. Pasinelli, R. H. Brown Jr., and D. Trotti, "Caspase-3 cleaves and inactivates the glutamate transporter EAAT2," The Journal of Biological Chemistry, vol. 281, no. 20, pp. 14076-14084, 2006.
20. A. Hartmann, S. Hunot, P. P. Michel et al., "Caspase-3: a vulnerability factor and final effector in apoptotic death of dopaminergic neurons in Parkinson's disease," Proceedings of the National Academy of Sciences of the United States of America, vol. 97, no. 6, pp. 2875-2880, 2000.
21. N. A. Tatton, "Increased caspase 3 and Bax immunoreactivity accompany nuclear GAPDH translocation and neuronal apoptosis in Parkinson's disease," Experimental Neurology, vol. 166, no. 1, pp. 29-43, 2000.
22. M. Chen, V. O. Ona, M. Lietal., "Minocycline inhibits caspase-1 and caspase-3 expression and delays mortality in a transgenic mouse model of Huntington disease," Nature Medicine, vol. 6, no. 7, pp. 797-801, 2000.
23. M. Tewari, L. T. Quan, K. O'Rourke et al., "Yama/CPP32β, a mammalian homolog of CED-3, is a CrmA-inhibitable protease that cleaves the death substrate poly(ADP-ribose) polymerase,"Cell, vol. 81, no. 5, pp. 801-809, 1995.
24. Y. J. Kim, Y. Yi, E. Sapp et al., "Caspase 3-cleaved N-terminal fragments of wild-type and mutant huntingtin are present in normal and Huntington's disease brains, associate with membranes, and undergo calpain-dependent proteolysis," Proceedings of the National Academy of Sciences of the United States of America, vol. 98, no. 22, pp. 12784-12789, 2001.
25. R. E. Castro, M. M. M. Santos, P. M. C. Glória et al., "Cell death targets and potential modulators in alzheimer's disease,"Current Pharmaceutical Design, vol. 16, no. 25, pp. 2851-2864, 2010.
26. M. Yamada, K. Kida, W. Amutuhaire, F. Ichinose, and M. Kaneki, "Gene disruption of caspase-3 prevents MPTP-induced Parkinson's disease in mice," Biochemical and Biophysical Research Communications, vol. 402, no. 2, pp. 312-318, 2010.
27. S. Toulmond, K. Tang, Y. Bureau et al., "Neuroprotective effects of M826, a reversible caspase-3 inhibitor, in the rat malonate model of Huntington's disease," British Journal of Pharmacology, vol. 141, no. 4, pp. 689-697, 2004.
28. P. Pasinelli and R. H. Brown, "Molecular biology of amyotrophic lateral sclerosis: insights from genetics," Nature Reviews Neuroscience, vol. 7, no. 9, pp. 710-723, 2006.
29. J. D. Rothstein, "Current hypotheses for the underlying biology of amyotrophic lateral sclerosis," Annals of Neurology, vol. 65, no. 1, pp. S3-S9, 2009.
30. S. Vukosavic, L. Stefanis, V. Jackson-Lewis et al., "Delaying caspase activation by Bcl-2: a clue to disease retardation in a transgenic mouse model of amyotrophic lateral sclerosis,"Journal of Neuroscience, vol. 20, no. 24, pp. 9119-9125, 2000.
31. R. M. Friedlander, "Apoptosis and caspases in neurodegenerative diseases," The New England Journal of Medicine, vol. 348, no. 14, pp. 1365-1375, 2003.
32. D. Szklarczyk, A. Franceschini, M. Kuhn et al., "The STRING database in 2011: functional interaction networks of proteins, globally integrated and scored," Nucleic Acids Research, vol. 39, no. 1, pp. D561-D568, 2011.
33. A. Franceschini, D. Szklarczyk, S. Frankild et al., "STRING v9.1: protein-protein interaction networks, with increased coverage and integration," Nucleic Acids Research, vol. 41, no. 1, pp. D808-D815, 2013.
34. M. L. Verdonk, J. C. Cole, M. J. Hartshorn, C. W. Murray, and R. D. Taylor, "Improved protein-ligand docking using GOLD,"Proteins: Structure, Function and Genetics, vol. 52, no. 4, pp. 609-623, 2003.
35. G. Jones, P. Willett, R. C. Glen, A. R. Leach, and R. Taylor, "Development and validation of a genetic algorithm for flexible docking," Journal of Molecular Biology, vol. 267, no. 3, pp. 727-748, 1997.
36. R. Wang, L. Lai, and S. Wang, "Further development and validation of empirical scoring functions for structure-based binding affinity prediction," Journal of Computer-Aided Molecular Design, vol. 16, no. 1, pp. 11-26, 2002.
37. S.-Y. Huang and X. Zou, "An iterative knowledge-based scoring function to predict protein-ligand interactions: II. Validation of the scoring function," Journal of Computational Chemistry, vol. 27, no. 15, pp. 1876-1882, 2006.
38. K. Vanommeslaeghe, E. Hatcher, C. Acharya et al., "STRING v9.1: protein-protein interaction networks, with increased coverage and integration," Journal of Computational Chemistry, vol. 31, no. 4, pp. 671-690, 2010.
39. M. Petersen and M. S. J. Simmonds, "Rosmarinic acid," Phytochemistry, vol. 62, no. 2, pp. 121-125, 2003.
40. F. Shaerzadeh, A. Ahmadiani, M. A. Esmaeili et al., "Antioxidant and antiglycating activities of Salvia sahendica and its protective effect against oxidative stress in neuron-like PC12 cells," Journal of Natural Medicines, vol. 65, no. 3-4, pp. 455-465, 2011.
41. T. Iuvone, D. de Filippis, G. Esposito, A. D'Amico, and A. A. Izzo, "The spice sage and its active ingredient rosmarinic acid protect PC12 cells from amyloid-β peptide-induced neurotoxicity,"Journal of Pharmacology and Experimental Therapeutics, vol. 317, no. 3, pp. 1143-1149, 2006.
42. R. M. Srivastava, S. Singh, S. K. Dubey, K. Misra, and A. Khar, "Immunomodulatory and therapeutic activity of curcumin,"International Immunopharmacology, vol. 11, no. 3, pp. 331-341, 2011.
43. T. Jiang, X.-L. Zhi, Y.-H. Zhang, L.-F. Pan, and P. Zhou, "Inhibitory effect of curcumin on the Al(III)-induced Aβ42aggregation and neurotoxicity in vitro," Biochimica et Biophysica Acta - Molecular Basis of Disease, vol. 1822, no. 8, pp. 1207-1215, 2012.
44. G. Seelinger, I. Merfort, and C. M. Schempp, "Anti-oxidant, anti-inflammatory and anti-allergic activities of luteolin,"Planta Medica, vol. 74, no. 14, pp. 1667-1677, 2008.
45. J. Pepping, "Huperzine A," The American Journal of Health-System Pharmacy, vol. 57, no. 6, pp. 533-534, 2000.
46. H. Y. Zhang and X. C. Tang, "Neuroprotective effects of huperzine A: new therapeutic targets for neurodegenerative disease," Trends in Pharmacological Sciences, vol. 27, no. 12, pp. 619-625, 2006.