Chitooligosaccharides protect rat cortical neurons against copper induced damage by attenuating intracellular level of reactive oxygen species.
A large number of evidence has suggests that dyshomeostasis of the redox-active biometals such as copper and other metal ions can lead to oxidative stress in neurons, which plays a key role in the pathology of neurodegenerative disorders. Chitooligosaccharides (COSs) are biodegradation product of chitosan and demonstrated diverse biological activities, Here we first report that protective effects of COSs (M.W. 1500, DD. 90%) against Cu(II) induced neurotoxicity in primary cultured rat cortical neurons. The toxicity of Cu(II) to cortical neurons was obviously attenuated in a concentration-dependent manner by COSs pretreated. The data derived from lactate dehydrogenase (LDH) release and the Hoechst 33342 assay support the results from MTT assay. After DCFH assay, COSs were found to depress Cu(II) induced elevation in intracellular reactive oxygen species (ROS), These findings suggest that COSs protect against Cu(II) induced neurotoxicity in primary cortical neurons by interfering with an increase in intracellular reactive oxygen species (ROS).
Xu
Wei
W
College of Arts and Science, Beijing Union University, Beijing 100191, China.
Huang
Han-chang
HC
Lin
Chang-jun
CJ
Jiang
Zhao-Feng
ZF
D000818:Animals; D002478:Cells, Cultured; D048271:Chitosan / Q000737:chemistry* / Q000494:pharmacology; D003300:Copper / Q000633:toxicity*; D045022:Lactate Dehydrogenases / Q000378:metabolism; D009474:Neurons / Q000187:drug effects*; D018696:Neuroprotective Agents / Q000737:chemistry* / Q000494:pharmacology; D018384:Oxidative Stress; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism*
D018696:Neuroprotective Agents; D017382:Reactive Oxygen Species; D003300:Copper; D048271:Chitosan; D045022:Lactate Dehydrogenases