Tags

Type your tag names separated by a space and hit enter

Nrf2/ARE Pathway Involved in Oxidative Stress Induced by Paraquat in Human Neural Progenitor Cells.
Oxid Med Cell Longev. 2016; 2016:8923860.OM

Abstract

Compelling evidences have shown that diverse environmental insults arising during early life can either directly lead to a reduction in the number of dopaminergic neurons or cause an increased susceptibility to neurons degeneration with subsequent environmental insults or with aging alone. Oxidative stress is considered the main effect of neurotoxins exposure. In this study, we investigated the oxidative stress effect of Paraquat (PQ) on immortalized human embryonic neural progenitor cells by treating them with various concentrations of PQ. We show that PQ can decrease the activity of SOD and CAT but increase MDA and LDH level. Furthermore, the activities of Cyc and caspase-9 were found increased significantly at 10 μM of PQ treatment. The cytoplasmic Nrf2 protein expressions were upregulated at 10 μM but fell back at 100 μM. The nuclear Nrf2 protein expressions were upregulated as well as the downstream mRNA expressions of HO-1 and NQO1 in a dose-dependent manner. In addition, the proteins expression of PKC and CKII was also increased significantly even at 1 μM. The results suggested that Nrf2/ARE pathway is involved in mild to moderate PQ-induced oxidative stress which is evident from dampened Nrf2 activity and low expression of antioxidant genes in PQ induced oxidative damage.

Authors+Show Affiliations

School of Public Health and Key Laboratory of Public Health Safety of the Ministry of Education, Fudan University, Shanghai 200032, China.School of Public Health and Key Laboratory of Public Health Safety of the Ministry of Education, Fudan University, Shanghai 200032, China.School of Public Health and Key Laboratory of Public Health Safety of the Ministry of Education, Fudan University, Shanghai 200032, China.School of Public Health and Key Laboratory of Public Health Safety of the Ministry of Education, Fudan University, Shanghai 200032, China.School of Public Health and Key Laboratory of Public Health Safety of the Ministry of Education, Fudan University, Shanghai 200032, China.School of Public Health and Key Laboratory of Public Health Safety of the Ministry of Education, Fudan University, Shanghai 200032, China.School of Public Health and Key Laboratory of Public Health Safety of the Ministry of Education, Fudan University, Shanghai 200032, China.School of Public Health and Key Laboratory of Public Health Safety of the Ministry of Education, Fudan University, Shanghai 200032, China.School of Public Health and Key Laboratory of Public Health Safety of the Ministry of Education, Fudan University, Shanghai 200032, China.

Pub Type(s)

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

Language

eng

PubMed ID

26649146

Citation

Dou, Tingting, et al. "Nrf2/ARE Pathway Involved in Oxidative Stress Induced By Paraquat in Human Neural Progenitor Cells." Oxidative Medicine and Cellular Longevity, vol. 2016, 2016, p. 8923860.
Dou T, Yan M, Wang X, et al. Nrf2/ARE Pathway Involved in Oxidative Stress Induced by Paraquat in Human Neural Progenitor Cells. Oxid Med Cell Longev. 2016;2016:8923860.
Dou, T., Yan, M., Wang, X., Lu, W., Zhao, L., Lou, D., Wu, C., Chang, X., & Zhou, Z. (2016). Nrf2/ARE Pathway Involved in Oxidative Stress Induced by Paraquat in Human Neural Progenitor Cells. Oxidative Medicine and Cellular Longevity, 2016, 8923860. https://doi.org/10.1155/2016/8923860
Dou T, et al. Nrf2/ARE Pathway Involved in Oxidative Stress Induced By Paraquat in Human Neural Progenitor Cells. Oxid Med Cell Longev. 2016;2016:8923860. PubMed PMID: 26649146.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nrf2/ARE Pathway Involved in Oxidative Stress Induced by Paraquat in Human Neural Progenitor Cells. AU - Dou,Tingting, AU - Yan,Mengling, AU - Wang,Xinjin, AU - Lu,Wen, AU - Zhao,Lina, AU - Lou,Dan, AU - Wu,Chunhua, AU - Chang,Xiuli, AU - Zhou,Zhijun, Y1 - 2015/11/15/ PY - 2015/06/11/received PY - 2015/07/08/accepted PY - 2015/12/10/entrez PY - 2015/12/10/pubmed PY - 2016/9/9/medline SP - 8923860 EP - 8923860 JF - Oxidative medicine and cellular longevity JO - Oxid Med Cell Longev VL - 2016 N2 - Compelling evidences have shown that diverse environmental insults arising during early life can either directly lead to a reduction in the number of dopaminergic neurons or cause an increased susceptibility to neurons degeneration with subsequent environmental insults or with aging alone. Oxidative stress is considered the main effect of neurotoxins exposure. In this study, we investigated the oxidative stress effect of Paraquat (PQ) on immortalized human embryonic neural progenitor cells by treating them with various concentrations of PQ. We show that PQ can decrease the activity of SOD and CAT but increase MDA and LDH level. Furthermore, the activities of Cyc and caspase-9 were found increased significantly at 10 μM of PQ treatment. The cytoplasmic Nrf2 protein expressions were upregulated at 10 μM but fell back at 100 μM. The nuclear Nrf2 protein expressions were upregulated as well as the downstream mRNA expressions of HO-1 and NQO1 in a dose-dependent manner. In addition, the proteins expression of PKC and CKII was also increased significantly even at 1 μM. The results suggested that Nrf2/ARE pathway is involved in mild to moderate PQ-induced oxidative stress which is evident from dampened Nrf2 activity and low expression of antioxidant genes in PQ induced oxidative damage. SN - 1942-0994 UR - https://www.unboundmedicine.com/medline/citation/26649146/Nrf2/ARE_Pathway_Involved_in_Oxidative_Stress_Induced_by_Paraquat_in_Human_Neural_Progenitor_Cells_ L2 - https://doi.org/10.1155/2016/8923860 DB - PRIME DP - Unbound Medicine ER -