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01 May 2018 : Laboratory Research

Curcumin Treatment is Associated with Increased Expression of the N-Methyl-D-Aspartate Receptor (NMDAR) Subunit, NR2A, in a Rat PC12 Cell Line Model of Alzheimer’s Disease Treated with the Acetyl Amyloid-β Peptide, Aβ(25–35)

Wei Qian1ABCDEFG, Haiyan Li2BCDE, Ningfeng Pan1EF, Changchun Zhang1ABCDEFG*

DOI: 10.12659/MSM.906933

Med Sci Monit 2018; 24: LBR2693-2699

Abstract

BACKGROUND: The aim of this study was to investigate the effect of curcumin treatment on the expression of the N-methyl-D-aspartate receptor (NMDAR) subunit, NR2A, in a rat PC12 cell line treated with the acetyl amyloid-β peptide, Aβ(25–35), in an in vitro model of Alzheimer’s disease.

MATERIAL AND METHODS: PC12 cells, derived from rat phaeochromocytoma, were treated for 24 hours with increasing concentrations of curcumin (5, 10, 20, 30 µM/L) in the presence of the acetyl amyloid-β peptide, Aβ(25–35). A Cell Counting Kit-8 (CCK-8) assay was used to determine cell viability, and flow cytometry was used to measure cell apoptosis. In the supernatant of the treated PC12 cells, Western blotting was used to measure the cell injury biomarker, lactate dehydrogenase (LDH), and the biomarker for oxidative stress, malondialdehyde (MDA). Expression of the N-methyl-D-aspartate receptor (NMDAR) subunit, NR2A, was analyzed by Western blotting and quantitative reverse transcription-polymerase chain reaction (qRT-PCR).

RESULTS: Curcumin treatment protected the rat PC12 cells from Ab(25–35)-induced reduction in cell viability, apoptosis, release of LDH, and MDA production. Curcumin treatment of PC12 cells was associated with increased expression of the NMDAR subunit, NR2A.

CONCLUSIONS: The findings of this study showed a neuroprotective effect of curcumin treatment in an in vitro model of Alzheimer’s disease that was associated with the increased expression of the NMDAR subunit, NR2A.

Keywords: Alzheimer Disease, Curcumin, Receptors, N-Methyl-D-Aspartate

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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750