Low-molecular-weight chondroitin sulfate attenuated injury by inhibiting oxidative stress in amyloid β-treated SH-SY5Y cells. Issue 14 (26th September 2018)

• Record Type: Journal Article
• Authors: Zhang, Qian; Na, Zhao; Cheng, Yanna; Wang, Fengshan
• Is Part Of: NeuroReport. Volume 29:Issue 14(2018)
• Publication Date: 2018-09-26
• Subjects: Alzheimer's disease -- amyloid-β protein -- chondroitin sulfate -- oxidative stress; Neurosciences -- Periodicals; Nervous system -- Periodicals; Neurophysiology -- Periodicals; Nervous System Diseases -- Periodicals; Nervous System Physiological Phenomena -- Periodicals; Neurosciences -- Periodicals; 616.805
• DOI: 10.1097/WNR.0000000000001092
• Languages: English
• ISSNs: 0959-4965

Abstract

Abstract : The neurotoxicity of aggregated amyloid β (Aβ) has been implicated as a critical cause in the pathogenesis of Alzheimer's disease. In a previous work, we have shown that low-molecular-weight chondroitin sulfate (LMWCS), a derivative of chondroitin sulfate, protected the SH-SY5Y neuroblastoma cells from Aβ25–35 -induced neurotoxicity, decreased intracellular reactive oxygen species level and inhibited the cell apoptosis. However, the underlying mechanism of the antioxidative effect of LMWCS in the SH-SY5Y cells has not been well explored. In the present study, the SH-SY5Y cells were cultured and exposed to 30 μM Aβ25–35 in the absence or presence of LMWCS (50, 100 and 200 μg/ml). Results indicate that incubation of cells with LMWCS before Aβ25–35 exposure increased superoxide dismutase, glutathione peroxidase and Na + /K + -ATPase activities and decreased the malondialdehyde content. In addition, LMWCS inhibited the imbalance of Bcl-2 and Bax and decreased caspase-3 and caspase-9 expressions. LMWCS antagonizes Aβ25–35 -induced neurotoxicity by attenuating oxidative stress, and our results suggest that LMWCS might be used as a potential compound for Alzheimer's disease prevention.