1. Upregulation of PPAR-gamma activity inhibits cyclooxygenase 2 expression in cortical neurons with N-methyl-d-aspartic acid induced excitatory neurotoxicity
- Author
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Qi-Fang Weng, Guo-Bin Chen, Min-Guang Xu, Ru-Tao Long, Han Wang, Xiao-Ying Wang, Chao-Na Jiang, and Xi-Nan Yi
- Subjects
ppar-γ ,nmda ,excitatory neurotoxicity ,cox-2 ,ca2+ concentrations ,Biotechnology ,TP248.13-248.65 - Abstract
This study aimed to investigate the effect of upregulated peroxisome proliferator-activated receptor-gamma (PPAR-γ) activity on cyclooxygenase 2 (COX-2) expression and N-methyl-d-aspartic acid (NMDA)-induced excitatory neurotoxicity in primary cultured cortical neurons. Rat cortical neurons were cultured for 8 days in vitro, and divided into control, NMDA, MK-801 (selective NMDA antagonist), rosiglitazone (ROSI, PPAR-γ agonist), GW9662 (PPAR-γ antagonist), NS398 (selective COX-2 antagonist) and NS398 + ROSI groups. Two hours after treatment in each group, cell viability, intracellular Ca2+ concentrations, PPAR-γ and COX-2 protein expression were detected by CCK-8 assay, flow cytometry and western blot assay, respectively. The results showed that compared with the control group, 100 μmol/L of NMDA significantly decreased the neuronal cell viability, increased Ca2+ concentrations, which also increased the COX-2 protein expression and decreased PPAR-γ expression in neurons. Compared with the NMDA group, the cell viability was increased, Ca2+ concentrations and COX-2 protein expression were significantly decreased, PPAR-γ expression was significantly increased in the MK-801, ROSI, NS398 and ROSI + NS398 groups (both P
- Published
- 2019
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