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Cytoprotective effect of polypeptide from Chlamys farreri on neuroblastoma (SH-SY5Y) cells following HO exposure involves scavenging ROS and inhibition JNK phosphorylation.
J Neurochem. 2009 Oct; 111(2):441-51.JN

Abstract

Oxidative stress has long been linked to cell death in many neurodegenerative conditions. Treatment with antioxidants is a promising approach for slowing disease progression. In this study, we used the neuroblastoma SH-SY5Y cells as an in vitro model to first assess the effect of polypeptide from Chlamys farreri (PCF), a natural marine antioxidant, on H(2)O(2)-induced neuronal cell death. Pre-treatment of SH-SY5Y cells with PCF inhibited H(2)O(2)-induced cell death in a concentration-dependent manner. In parallel, intracellular reactive oxygen species generation and lipid peroxidation were inhibited by PCF. Under severe H(2)O(2) insult, PCF promoted endogenous antioxidant defense components including glutathione peroxidase, catalase, superoxide dismutase, and glutathione. PCF also protected DNA from oxidative damage and enhanced the removal of 8-oxo-7,8-dihydro-2'-deoxyguanosine from DNA. Further, we found that PCF potentially prevented H(2)O(2)-induced cell apoptosis. When investigated mitogen-activated protein kinase signaling pathway, we found that pre-treatment of cells with PCF significantly blocked H(2)O(2)-induced phosphorylation of c-Jun N-terminal kinase of the mitogen-activated protein kinase family. However, PCF had little inhibitory effect on the H(2)O(2)-induced activation of extracellular signal-regulated kinase. Taken together, these data demonstrate that PCF prevents oxidative stress-induced reactive oxygen species production and c-Jun N-terminal kinase activation and may be useful in the treatment of neurodegenerative diseases.

Authors+Show Affiliations

Department of Molecular Biology, School of Medicine and Pharmacy, Ocean University of China, Qingdao, China. yejunli126@126.comNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19682211

Citation

Ye, Junli, et al. "Cytoprotective Effect of Polypeptide From Chlamys Farreri On Neuroblastoma (SH-SY5Y) Cells Following HO Exposure Involves Scavenging ROS and Inhibition JNK Phosphorylation." Journal of Neurochemistry, vol. 111, no. 2, 2009, pp. 441-51.
Ye J, Han Y, Wang C, et al. Cytoprotective effect of polypeptide from Chlamys farreri on neuroblastoma (SH-SY5Y) cells following HO exposure involves scavenging ROS and inhibition JNK phosphorylation. J Neurochem. 2009;111(2):441-51.
Ye, J., Han, Y., Wang, C., & Yu, W. (2009). Cytoprotective effect of polypeptide from Chlamys farreri on neuroblastoma (SH-SY5Y) cells following HO exposure involves scavenging ROS and inhibition JNK phosphorylation. Journal of Neurochemistry, 111(2), 441-51. https://doi.org/10.1111/j.1471-4159.2009.06328.x
Ye J, et al. Cytoprotective Effect of Polypeptide From Chlamys Farreri On Neuroblastoma (SH-SY5Y) Cells Following HO Exposure Involves Scavenging ROS and Inhibition JNK Phosphorylation. J Neurochem. 2009;111(2):441-51. PubMed PMID: 19682211.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cytoprotective effect of polypeptide from Chlamys farreri on neuroblastoma (SH-SY5Y) cells following HO exposure involves scavenging ROS and inhibition JNK phosphorylation. AU - Ye,Junli, AU - Han,Yantao, AU - Wang,Chunbo, AU - Yu,Wengong, Y1 - 2009/08/03/ PY - 2009/8/18/entrez PY - 2009/8/18/pubmed PY - 2009/10/23/medline SP - 441 EP - 51 JF - Journal of neurochemistry JO - J Neurochem VL - 111 IS - 2 N2 - Oxidative stress has long been linked to cell death in many neurodegenerative conditions. Treatment with antioxidants is a promising approach for slowing disease progression. In this study, we used the neuroblastoma SH-SY5Y cells as an in vitro model to first assess the effect of polypeptide from Chlamys farreri (PCF), a natural marine antioxidant, on H(2)O(2)-induced neuronal cell death. Pre-treatment of SH-SY5Y cells with PCF inhibited H(2)O(2)-induced cell death in a concentration-dependent manner. In parallel, intracellular reactive oxygen species generation and lipid peroxidation were inhibited by PCF. Under severe H(2)O(2) insult, PCF promoted endogenous antioxidant defense components including glutathione peroxidase, catalase, superoxide dismutase, and glutathione. PCF also protected DNA from oxidative damage and enhanced the removal of 8-oxo-7,8-dihydro-2'-deoxyguanosine from DNA. Further, we found that PCF potentially prevented H(2)O(2)-induced cell apoptosis. When investigated mitogen-activated protein kinase signaling pathway, we found that pre-treatment of cells with PCF significantly blocked H(2)O(2)-induced phosphorylation of c-Jun N-terminal kinase of the mitogen-activated protein kinase family. However, PCF had little inhibitory effect on the H(2)O(2)-induced activation of extracellular signal-regulated kinase. Taken together, these data demonstrate that PCF prevents oxidative stress-induced reactive oxygen species production and c-Jun N-terminal kinase activation and may be useful in the treatment of neurodegenerative diseases. SN - 1471-4159 UR - https://www.unboundmedicine.com/medline/citation/19682211/Cytoprotective_effect_of_polypeptide_from_Chlamys_farreri_on_neuroblastoma__SH_SY5Y__cells_following_HO_exposure_involves_scavenging_ROS_and_inhibition_JNK_phosphorylation_ L2 - https://doi.org/10.1111/j.1471-4159.2009.06328.x DB - PRIME DP - Unbound Medicine ER -