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Rosiglitazone protects human neuroblastoma SH-SY5Y cells against MPP+ induced cytotoxicity via inhibition of mitochondrial dysfunction and ROS production.
J Neurol Sci. 2007 Feb 15; 253(1-2):53-60.JN

Abstract

1-Methyl-4-phenylpyridinium ion (MPP(+)), an inhibitor of mitochondrial complex I, has been widely used as a neurotoxin because it elicits a severe Parkinson's disease-like syndrome with elevation of intracellular reactive oxygen species (ROS) level and apoptotic death. Rosiglitazone, a peroxisome proliferator-activated receptor (PPAR)-gamma agonist, has been known to show various non-hypoglycemic effects, including anti-inflammatory, anti-atherogenic, and anti-apoptotic. In the present study, we investigated the protective effects of rosiglitazone on MPP(+) induced cytotoxicity in human neuroblastoma SH-SY5Y cells, as well as underlying mechanism. Our results suggested that the protective effects of rosiglitazone on MPP(+) induced apoptosis may be ascribed to its anti-oxidative properties, anti-apoptotic activity via inducing expression of SOD and catalase and regulating the expression of Bcl-2 and Bax. These data indicated that rosiglitazone might provide a valuable therapeutic strategy for the treatment of progressive neurodegenerative disease such as Parkinson's disease.

Authors+Show Affiliations

The Brain Korea 21 Project for Medical Science, Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo 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

17266988

Citation

Jung, Tae Woo, et al. "Rosiglitazone Protects Human Neuroblastoma SH-SY5Y Cells Against MPP+ Induced Cytotoxicity Via Inhibition of Mitochondrial Dysfunction and ROS Production." Journal of the Neurological Sciences, vol. 253, no. 1-2, 2007, pp. 53-60.
Jung TW, Lee JY, Shim WS, et al. Rosiglitazone protects human neuroblastoma SH-SY5Y cells against MPP+ induced cytotoxicity via inhibition of mitochondrial dysfunction and ROS production. J Neurol Sci. 2007;253(1-2):53-60.
Jung, T. W., Lee, J. Y., Shim, W. S., Kang, E. S., Kim, S. K., Ahn, C. W., Lee, H. C., & Cha, B. S. (2007). Rosiglitazone protects human neuroblastoma SH-SY5Y cells against MPP+ induced cytotoxicity via inhibition of mitochondrial dysfunction and ROS production. Journal of the Neurological Sciences, 253(1-2), 53-60.
Jung TW, et al. Rosiglitazone Protects Human Neuroblastoma SH-SY5Y Cells Against MPP+ Induced Cytotoxicity Via Inhibition of Mitochondrial Dysfunction and ROS Production. J Neurol Sci. 2007 Feb 15;253(1-2):53-60. PubMed PMID: 17266988.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Rosiglitazone protects human neuroblastoma SH-SY5Y cells against MPP+ induced cytotoxicity via inhibition of mitochondrial dysfunction and ROS production. AU - Jung,Tae Woo, AU - Lee,Ji Young, AU - Shim,Wan Sub, AU - Kang,Eun Seok, AU - Kim,Soo Kyung, AU - Ahn,Chul Woo, AU - Lee,Hyun Chul, AU - Cha,Bong Soo, Y1 - 2007/01/30/ PY - 2006/06/20/received PY - 2006/11/09/revised PY - 2006/11/22/accepted PY - 2007/2/3/pubmed PY - 2007/4/19/medline PY - 2007/2/3/entrez SP - 53 EP - 60 JF - Journal of the neurological sciences JO - J Neurol Sci VL - 253 IS - 1-2 N2 - 1-Methyl-4-phenylpyridinium ion (MPP(+)), an inhibitor of mitochondrial complex I, has been widely used as a neurotoxin because it elicits a severe Parkinson's disease-like syndrome with elevation of intracellular reactive oxygen species (ROS) level and apoptotic death. Rosiglitazone, a peroxisome proliferator-activated receptor (PPAR)-gamma agonist, has been known to show various non-hypoglycemic effects, including anti-inflammatory, anti-atherogenic, and anti-apoptotic. In the present study, we investigated the protective effects of rosiglitazone on MPP(+) induced cytotoxicity in human neuroblastoma SH-SY5Y cells, as well as underlying mechanism. Our results suggested that the protective effects of rosiglitazone on MPP(+) induced apoptosis may be ascribed to its anti-oxidative properties, anti-apoptotic activity via inducing expression of SOD and catalase and regulating the expression of Bcl-2 and Bax. These data indicated that rosiglitazone might provide a valuable therapeutic strategy for the treatment of progressive neurodegenerative disease such as Parkinson's disease. SN - 0022-510X UR - https://www.unboundmedicine.com/medline/citation/17266988/Rosiglitazone_protects_human_neuroblastoma_SH_SY5Y_cells_against_MPP+_induced_cytotoxicity_via_inhibition_of_mitochondrial_dysfunction_and_ROS_production_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0022-510X(06)00539-9 DB - PRIME DP - Unbound Medicine ER -