Curcumin (Record no. 9777)

MARC details
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fixed length control field a
003 - CONTROL NUMBER IDENTIFIER
control field OSt
005 - DATE AND TIME OF LATEST TRANSACTION
control field 20191019101011.0
008 - FIXED-LENGTH DATA ELEMENTS--GENERAL INFORMATION
fixed length control field 191019b xxu||||| |||| 00| 0 eng d
040 ## - CATALOGING SOURCE
Original cataloging agency AIKTC-KRRC
Transcribing agency AIKTC-KRRC
100 ## - MAIN ENTRY--PERSONAL NAME
9 (RLIN) 9973
Author Hui-Yin, Yow
245 ## - TITLE STATEMENT
Title Curcumin
Remainder of title :The Molecular Mechanisms of Action in Inflammation and Cell Death during Kainate-Induced Epileptogenesis
250 ## - EDITION STATEMENT
Volume, Issue number Vol.52(1), Jan-Mar
260 ## - PUBLICATION, DISTRIBUTION, ETC.
Place of publication, distribution, etc. Karnataka
Name of publisher, distributor, etc. Indian journal of pharmaceutical education and research
Year 2018
300 ## - PHYSICAL DESCRIPTION
Pagination 32-41p.
520 ## - SUMMARY, ETC.
Summary, etc. Background: 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 - SUBJECT ADDED ENTRY--TOPICAL TERM
9 (RLIN) 4639
Topical term or geographic name entry element PHARMACEUTICS
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9 (RLIN) 9974
Co-Author Nurulumi Ahmad
773 0# - HOST ITEM ENTRY
International Standard Serial Number 0019-5464
Title Indian journal of pharmaceutical education and research
Place, publisher, and date of publication Bengluru Association of Pharmaceutical Teachers of India (APTI)
856 ## - ELECTRONIC LOCATION AND ACCESS
URL https://www.ijper.org/sites/default/files/IndJPhaEdRes_52_1_32.pdf
Link text Click here
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Source of classification or shelving scheme Dewey Decimal Classification
Koha item type Articles Abstract Database
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    Dewey Decimal Classification     School of Pharmacy School of Pharmacy Archieval Section 19/10/2019   2019930 19/10/2019 19/10/2019 Articles Abstract Database
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