| 000 | a | ||
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| 999 |
_c9777 _d9777 |
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| 003 | OSt | ||
| 005 | 20191019101011.0 | ||
| 008 | 191019b xxu||||| |||| 00| 0 eng d | ||
| 040 |
_aAIKTC-KRRC _cAIKTC-KRRC |
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| 100 |
_99973 _aHui-Yin, Yow |
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| 245 |
_aCurcumin _b:The Molecular Mechanisms of Action in Inflammation and Cell Death during Kainate-Induced Epileptogenesis |
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| 250 | _aVol.52(1), Jan-Mar | ||
| 260 |
_aKarnataka _bIndian journal of pharmaceutical education and research _c2018 |
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| 300 | _a32-41p. | ||
| 520 | _aBackground: Recent preclinical studies demonstrated the potential antiepileptogenic effect of curcumin. Its molecular pathways in modulating epileptogenesis remain unclear. Objectives: This study investigated the epileptogenic processes induced by kainic acid (KA) and to investigate the antiepileptogenic pathways associated with curcumin therapy. Methods: A single dose of KA 10 mg/kg was used to induce a convulsive status epilepticus in female Wistar rats. After one week of curcumin treatment, gene expression profiling by using microarray was conducted on hippocampal tissues. A set of differential expression changes was determined based on criteria of dual fold change in either direction and p < 0.05, whereas gene annotation and pathway analysis had been performed using Database for Annotation, Visualization and Integrated Discovery software. Results: A number of genes significantly altered in expression during KA-induced epileptogenesis. Inflammation and immune response were the prominent over-expressed processes induced by KA. Genes of cell surface molecule (CD74), cytokines and immune response related genes (IL18, IFNGR1, C3, RT1-BA) were significantly up-regulated. Changes of genes related to cell death and gliosis (NCSTN, CTSH) were also observed in KA-induced epileptogenesis. This study revealed that curcumin modulated the epileptogenic process by up-regulating genes related to antiinflammatory cytokines (IL10RB, CXCL16, and CXCL17) and protecting against cell loss by up-regulating NCSTN. It was also likely to exert neuroprotective effects through the up-regulation of CX3CL1 and CXCL16. Conclusion: This study provides novel insights into the mechanisms of curcumin in epileptic brain, which form the basis for future studies looking into its molecular pathway as an antiepileptogenic agent. | ||
| 650 | 0 |
_94639 _aPHARMACEUTICS |
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| 700 |
_99974 _aNurulumi Ahmad |
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| 773 | 0 |
_x0019-5464 _tIndian journal of pharmaceutical education and research _dBengluru Association of Pharmaceutical Teachers of India (APTI) |
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| 856 |
_uhttps://www.ijper.org/sites/default/files/IndJPhaEdRes_52_1_32.pdf _yClick here |
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| 942 |
_2ddc _cAR |
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