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Protective effects of curcumin on acrolein-induced neurotoxicity in HT22 mouse hippocampal cells
Authors:Lan-Ying Shi  Li Zhang  Hui Li  Tao-Li Liu  Ji-Cai Lai  Zhi-Bing Wu  Jian Qin
Affiliation:1. Department of Traditional Chinese Medicine, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China;2. Department of Traditional Chinese Medicine, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, China;3. Department of Neurology, The First Clinical Medical College of Guangzhou University of Chinese Medicine, Guangzhou, China
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 25 μM acrolein for 24 h with or without pre-treating with curcumin at the selected optimum concentration (5 μg/mL) for 30 min. 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.
Keywords:AD  Alzheimer disease  A  amyloid-beta peptide  ADAM-10  A-disintegrin and metalloprotease 10  APP  amyloid precursor protein  GFAP  glial fibrillary acidic protein  MAPK  mitogen-activated protein kinase  MDA  malondialdehyde  MWM  Morris water maze  NEP  neprilysin  LR-11/SorLA  sortilin-related receptor  LRP-1  low density lipoprotein receptor related protein-1  RAGE  receptor for advanced glycation end products  ROS  reactive oxygen species  SOD  superoxide dismutase  Curcumin  Acrolein  Alzheimer disease  BNDF/TrkB
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