Chitosan oligosaccharides protect rat primary hippocampal neurons from oligomeric β-amyloid 1-42-induced neurotoxicity
| Autor: | Yaxuan Sun, Wenjuan Liu, Qingzhu Zhu, Zhao-Feng Jiang, Ping Chang, Xueling Dai, Shigong Zhu |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
Programmed cell death
Cell Survival Primary Cell Culture Oligosaccharides Biology Hippocampus Neuroprotection Lipid peroxidation chemistry.chemical_compound medicine Amyloid precursor protein Animals Viability assay Senile plaques Phosphorylation Neurons chemistry.chemical_classification Chitosan Reactive oxygen species Amyloid beta-Peptides Caspase 3 General Neuroscience JNK Mitogen-Activated Protein Kinases Neurotoxicity medicine.disease Peptide Fragments Rats Oxidative Stress Biochemistry chemistry biology.protein Lipid Peroxidation Reactive Oxygen Species |
| Zdroj: | Neuroscience Letters. 554:64-69 |
| ISSN: | 0304-3940 |
| DOI: | 10.1016/j.neulet.2013.08.046 |
| Popis: | β-Amyloid peptide (Aβ), the major component of senile plaques in patients with Alzheimer's disease (AD), is believed to facilitate the progressive neurodegeneration that occurs in this disease. Mounting natural compounds are proved to be potential candidates for the prevention and treatment of AD. Chitosan oligosaccharides (COSs), the enzymatic hydrolysates of chitosan, have been reported to possess diverse biological activities. Here we investigated the effect of COSs on oligomeric Aβ-mediated toxicity in rat primary hippocampal neurons. Pretreatment with COSs markedly inhibited cell death induced by Aβ exposure as determined by cell viability assay and lactate dehydrogenase release assay. In parallel, the generation of reactive oxygen species and lipid peroxidation were attenuated by COSs. Furthermore, our results indicated that COSs remarkably prevented Aβ-induced cell apoptosis as manifested by depressing the elevation of Bax/Bcl-2 ratio and caspase-3 activation, suggesting that the neuroprotective effect of COSs could be partially due to apoptosis regulation. In addition, pretreatment with COSs significantly blocked Aβ-induced phosphorylation of c-Jun N-terminal kinase. Taken together, these findings may shed light on the role of COSs as a potential therapeutic agent for AD. |
| Databáze: | OpenAIRE |
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