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Protective Effects of Resolvin D1 Against-Amyloid1-42-Induced Neurotoxicity in Rat PC-12 Cells

Author: GongXia
Tutor: TangYong
School: Chongqing Medical University
Course: Human Anatomy,Histology and Embryology
Keywords: Alzheimer’s disease (AD) amyloid-beta (Aβ) Resolvin D1 (RvD1) HO-1 AKT
CLC: R965
Type: Master's thesis
Year: 2011
Downloads: 106
Quote: 0
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Abstract


Objective: Alzheimer’s disease (AD) is the most common age-related neurodegenerative disorder syndrome. Excessive accumulation of amyloid-beta (Aβ) peptide has been implicated as a pivotal event in the pathogenesis of AD. Possible mechanisms involving Aβ-induced neuronal cytotoxicity include excess production of reactive oxidative species (ROS), which lead to neuronal apoptosis. Thereby, Searching for the ways to prevent Aβ1?42-induced neuronal cytotoxicity is very important for developing effective therapeutic strategy of AD. Numerous epidemiological, clinical, animal or cellular studies indicate thatω?3 polyunsaturated fatty acid docosahexaenoic acid (DHA) is an important neuroprotective substance that prevents AD as well as other age-related neurodegenerative diseases. Recently, Resolvin D1 (RvD1), an endogenous lipid molecule derived from DHA, has been comprehensive focused on as its extensive and efficient biological properties. In this study, we investigated the mechanisms and effects of RvD1 on Aβ1?42-induced neuronal cytotoxicity. Methods: The differentiated neuronal-like PC12 cells were treated with 50μM Aβ1?42 in the presence or absence of RvD1 (1, 10, 100 nM, respectively) with or without Wortmannin (200 nM). Cells were collected 48 h after Aβ1?42 treatment. Cells viability was measured with MTT. Cells apoptosis was assayed with FCM and Fluorescence microscope. ROS and mitochondrial transmembrane potential (MTP) was determined with FCM. Cytochrome C was assayed with ELISA. Caspase 3 activity was measured with microplate. Bax, Bcl-2, P-AKT and HO-1 were determined with western blotting.Results: Compared with Control group, Aβ1?42 treatment significantly decreased the cell viability, increased cell apoptosis, enhanced ROS production, and lowed MTP, promoted caspase 3 activities and cytochrome C releases, down-regulated Bcl-2 protein expression, up-regulated Bax protein expression. However, RvD1 (1, 10, 100 nM) concentration-dependently protected the differentiated neuronal-like PC12 cells from Aβ1?42-induced neurotoxicity. Interestingly, RvD1 also dose-dependently enhanced P-AKT and HO-1 expression. Further, Wortmannin (200 nM), a specific PI3K kinase inhibitor, not only blocked AKT phosphorylation and HO-1 expression, but also reversed these beneficial effects of RvD1 on Aβ1?42-induced neurotoxicity.Conclusion: RvD1 could effectively prevent Aβ1?42-induced neurotoxicity in differentiated neuronal-like PC12 cells, including enhanced cell viability, inhibited cell apoptosis, reduced ROS production and increased MTP, decreased cytochrome C release, down-regulated Bax and up-regulated Bcl-2 expression. The underlying mechanisms might be related to PI3K/AKT signaling and HO-1 expression.

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