1. Protective effects of curcumin on acrolein-induced neurotoxicity in HT22 mouse hippocampal cells.
- Author
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Shi LY, Zhang L, Li H, Liu TL, Lai JC, Wu ZB, and Qin J
- Subjects
- Amyloid Precursor Protein Secretases metabolism, Amyloid beta-Protein Precursor biosynthesis, Animals, Apoptosis drug effects, Brain-Derived Neurotrophic Factor metabolism, Cell Survival drug effects, Cells, Cultured, Disintegrins metabolism, Glutathione metabolism, Malondialdehyde metabolism, Membrane Glycoproteins metabolism, Metalloproteases metabolism, Mice, Protein-Tyrosine Kinases metabolism, Receptor for Advanced Glycation End Products metabolism, Superoxide Dismutase metabolism, Acrolein antagonists & inhibitors, Acrolein toxicity, Curcumin pharmacology, Hippocampus cytology, Neuroprotective Agents pharmacology
- Abstract
Background: Aging is one of the most important inevitable risk factors of Alzheimer disease (AD). Oxidative stress plays a critical role in the process of aging. Curcumin has been proposed to improve neural damage, especially neurodegenerative injury, through its antioxidant and anti-inflammatory properties. Therefore, we investigated the effects of curcumin on acrolein-induced AD-like pathologies in HT22 cells., Methods: HT22 murine hippocampal neuronal cells were treated with 25μM acrolein for 24h with or without pre-treating with curcumin at the selected optimum concentration (5μg/mL) for 30min. Cell viability and apoptosis were measured by CCK8 assay and flow cytometric analysis. Levels of glutathione (GSH), superoxide dismutase (SOD), and malondialdehyde (MDA) were detected by a GSH assay kit or commercial assay kits, respectively. Alterations in the expression of BDNF/TrkB and key enzymes involved in amyloid precursor protein (APP) metabolism were assessed by western blotting., Results: Data showed that curcumin significantly reversed acrolein-induced oxidative stress indicated by depletion of GSH and SOD, and elevation of MDA. The findings also suggested curcumin's potential in protecting HT22 cells against acrolein through regulating the BDNF/TrkB signaling. In addition, acrolein-induced reduction in A-disintegrin and metalloprotease, and the increase of amyloid precursor protein, β-secretase, and receptor for advanced glycation end products were reversed either, and most of them were nearly restored to the control levels by curcumin., Conclusion: These findings demonstrate the protective effects of curcumin on acrolein-induced neurotoxicity in vitro, which further suggests its potential role in the treatment of AD., (Copyright © 2018. Published by Elsevier B.V.)
- Published
- 2018
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