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Prostaglandin analogue misoprostol attenuates neurotoxin 1-methyl-4-phenylpyridinium-induced mitochondrial damage and cell death in differentiated PC12 cells.
Brain Res Bull. 2008 Nov 25; 77(5):293-300.BR

Abstract

Defects in mitochondrial function have been shown to participate in the induction of neuronal cell injury. The present study assessed the preventive effect of a prostaglandin E(1) analogue misoprostol against the toxicity of parkinsonian neurotoxin 1-methyl-4-phenylpyridinium (MPP(+)) with respect to the mitochondria-mediated cell death process and oxidative stress. MPP(+) induced the nuclear damage, the changes in the mitochondrial membrane permeability, the formation of reactive oxygen species and the depletion of GSH, which leads to cell death in differentiated PC12 cells. Misoprostol prevented the toxic effect of MPP(+). Treatment with misoprostol significantly attenuated the MPP(+)-induced mitochondrial membrane permeability change that leads to the increase in pro-apoptotic Bax and Cytochrome c levels, and subsequent caspase-3 activation. The protective effect of misoprostol may be supported by the inhibitory effect of prostaglandin E(1) on the MPP(+) toxicity. Misoprostol significantly attenuated another parkinsonian neurotoxin rotenone-induced cell death. The results show that misoprostol may prevent the MPP(+) toxicity by suppressing the mitochondrial membrane permeability change that leads to the Cytochrome c release and caspase-3 activation. The preventive effect seems to be ascribed to the inhibitory effect on the formation of reactive oxygen species and depletion of GSH.

Authors+Show Affiliations

Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul 156-756, South Korea.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18602972

Citation

Choi, Eun Joo, et al. "Prostaglandin Analogue Misoprostol Attenuates Neurotoxin 1-methyl-4-phenylpyridinium-induced Mitochondrial Damage and Cell Death in Differentiated PC12 Cells." Brain Research Bulletin, vol. 77, no. 5, 2008, pp. 293-300.
Choi EJ, Han JH, Lee CS. Prostaglandin analogue misoprostol attenuates neurotoxin 1-methyl-4-phenylpyridinium-induced mitochondrial damage and cell death in differentiated PC12 cells. Brain Res Bull. 2008;77(5):293-300.
Choi, E. J., Han, J. H., & Lee, C. S. (2008). Prostaglandin analogue misoprostol attenuates neurotoxin 1-methyl-4-phenylpyridinium-induced mitochondrial damage and cell death in differentiated PC12 cells. Brain Research Bulletin, 77(5), 293-300. https://doi.org/10.1016/j.brainresbull.2008.06.006
Choi EJ, Han JH, Lee CS. Prostaglandin Analogue Misoprostol Attenuates Neurotoxin 1-methyl-4-phenylpyridinium-induced Mitochondrial Damage and Cell Death in Differentiated PC12 Cells. Brain Res Bull. 2008 Nov 25;77(5):293-300. PubMed PMID: 18602972.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Prostaglandin analogue misoprostol attenuates neurotoxin 1-methyl-4-phenylpyridinium-induced mitochondrial damage and cell death in differentiated PC12 cells. AU - Choi,Eun Joo, AU - Han,Jeong Ho, AU - Lee,Chung Soo, Y1 - 2008/07/09/ PY - 2008/06/06/received PY - 2008/06/08/revised PY - 2008/06/09/accepted PY - 2008/7/8/pubmed PY - 2011/3/4/medline PY - 2008/7/8/entrez SP - 293 EP - 300 JF - Brain research bulletin JO - Brain Res Bull VL - 77 IS - 5 N2 - Defects in mitochondrial function have been shown to participate in the induction of neuronal cell injury. The present study assessed the preventive effect of a prostaglandin E(1) analogue misoprostol against the toxicity of parkinsonian neurotoxin 1-methyl-4-phenylpyridinium (MPP(+)) with respect to the mitochondria-mediated cell death process and oxidative stress. MPP(+) induced the nuclear damage, the changes in the mitochondrial membrane permeability, the formation of reactive oxygen species and the depletion of GSH, which leads to cell death in differentiated PC12 cells. Misoprostol prevented the toxic effect of MPP(+). Treatment with misoprostol significantly attenuated the MPP(+)-induced mitochondrial membrane permeability change that leads to the increase in pro-apoptotic Bax and Cytochrome c levels, and subsequent caspase-3 activation. The protective effect of misoprostol may be supported by the inhibitory effect of prostaglandin E(1) on the MPP(+) toxicity. Misoprostol significantly attenuated another parkinsonian neurotoxin rotenone-induced cell death. The results show that misoprostol may prevent the MPP(+) toxicity by suppressing the mitochondrial membrane permeability change that leads to the Cytochrome c release and caspase-3 activation. The preventive effect seems to be ascribed to the inhibitory effect on the formation of reactive oxygen species and depletion of GSH. SN - 1873-2747 UR - https://www.unboundmedicine.com/medline/citation/18602972/Prostaglandin_analogue_misoprostol_attenuates_neurotoxin_1_methyl_4_phenylpyridinium_induced_mitochondrial_damage_and_cell_death_in_differentiated_PC12_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0361-9230(08)00227-X DB - PRIME DP - Unbound Medicine ER -