Inhibitory effects of short-term administration of dl-α-lipoic acid on oxidative vulnerability induced by Aβ amyloid fibrils (25–35) in mice

被引:0
作者
E. Philip Jesudason
J. Gunasingh Masilamoni
Ben S. Ashok
B’joe Baben
V. Arul
K. Samuel Jesudoss
W. Charles E. Jebaraj
S. Dhandayuthapani
S. Vignesh
R. Jayakumar
机构
[1] Central Leather Research Institute,Bio
[2] Sri Ramachandra Medical College and Research Institute (Deemed University),Organic and Neurochemistry Laboratory
[3] Sri Ramachandra Medical College and Research Institute (Deemed University),Department of Biochemistry
[4] Stanford University,Department of Biotechnology
来源
Molecular and Cellular Biochemistry | 2008年 / 311卷
关键词
Aβ amyloid; -α-lipoic acid; Reactive oxygen species; Enzymic and non-enzymic antioxidants; ATPase; Glial fibrillary acidic protein; Nuclear factor kappa-B;
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摘要
Aβ amyloid peptide is believed to induce oxidative stress leading to inflammation, which is postulated to play a significant role in the toxicity of Alzheimer’s disease (AD). This study was designed to investigate the inhibitory effects of dl-α lipoic acid (LA), a potential free radical scavenger, on oxidative vulnerability induced by intraperitoneal injection of Aβ25–35 amyloid fibrils in mice. Mice were divided into three groups: control, Aβ amyloid toxicity induced (AT), and LA treated (ATL). Blood Plasma was separated, liver, spleen and brain were dissected and analysis of oxidants, antioxidants, ATPases, glial fibrillary acidic protein (GFAP) and nuclear factor kappa-B (NFκB) were carried out. Results show biochemical parameters such as reactive oxygen species (ROS) and lipid peroxidation (LPO) were significantly lowered (P < 0.05) and levels of antioxidants and ATPase (P < 0.05) were significantly increased (P < 0.05) in hepatocytes, splenocytes and astrocytes of the ATL group. Moreover, our histological results revealed a decreased GFAP immunoreactivity in the neocortical region and NFκB immunoreactivity in neocortex, liver and spleen. This study reiterates LA as a potent free radical scavenger to combat oxidative vulnerability in the treatment for Aβ amyloid toxicity.
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页码:145 / 156
页数:11
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