Journal
NEUROCHEMICAL RESEARCH
Volume 40, Issue 7, Pages 1509-1519Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-015-1628-8
Keywords
Chondroitin sulfate; Reactive oxygen species; Antioxidant; Apoptosis; Mitochondrial dysfunctions
Categories
Funding
- National Natural Science Fund [81441094]
- Natural Science Foundation of Shandong Province [ZR2013HQ010]
- Medical Scientific Foundation of Shandong Province [2013WS0256]
- Qingdao Municipal Science and Technology Foundation [13-1-3-48-nsh]
- National Postdoctoral Research Project [2015M571999]
- Qingdao Postdoctoral Research Project
- Young Foundation of Qingdao University
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The purpose of the study was to investigate the protective effect and molecular mechanism of chondroitin sulfate (CS) against 6-hydroxydopamine (6-OHDA) induced toxicity in the human neuroblastoma cell line SH-SY5Y. The results showed that CS could protect SH-SY5Y cells against 6-OHDA-induced injury. The subsequent mechanism study showed that the anti-oxidation of CS may partly be mediated through inhibiting the intracellular reactive oxygen species overproduction, recovering the reduction of nuclear NF-E2-related factor-2 (Nrf2) expression and the reduction of antioxidants activity induced by 6-OHDA. Furthermore, CS pretreatment significantly attenuated 6-OHDA-induced cell apoptosis and nuclear condensation. 6-OHDA-induced dysfunctions, including the decrease of mitochondrial membrane potential (Delta Im), increase of intracellular free Ca2+, imbalance of Bcl-2/Bax ratio, release of Cyt-c from the mitochondria and activation of caspase-3 and caspase-9 were attenuated by CS pretreatment, which demonstrated that CS suppressed 6-OHDA-induced apoptosis in SH-SY5Y cells possibly through mitochondria protection. These results suggest that CS exhibits anti-oxidation through the up-regulation of Nrf2 along with endogenous antioxidant, and reduces apoptosis via inhibiting the mitochondrial pathway to protect SH-SY5Y cells damaged by 6-OHDA.
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