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Edaravone protects against MPP+ -induced cytotoxicity in rat primary cultured astrocytes via inhibition of mitochondrial apoptotic pathway.
J Neurochem. 2008 Sep; 106(6):2345-52.JN

Abstract

Edaravone (Eda) is a potent scavenger of hydroxyl radicals and has been demonstrated to be beneficial for patients with acute ischemic stroke. This study was set out to investigate whether Eda protect against MPP(+)-induced cytotoxicity in rat primary cultured astrocytes. The results showed that pre-treatment with Eda inhibited astrocytic apoptosis and lactate dehydrogenase release induced by MPP(+) (200 microM). Further study revealed that Eda prevented GSH depletion, down-regulated mRNA expressions of NADPH oxidase membrane subunit gp91 and membrane-translocated subunit p47, and prevented the decreases of state 3 respiration respiration and respiratory control ratio induced by MPP(+), and thereby inhibited reactive oxygen species production evoked by MPP(+). Moreover, Eda could ameliorate mitochondrial respiratory function, restrain, and prevent mitochondrial membrane potential loss induced by MPP(+). Consequently, Eda inhibited releases of cytochrome c and apoptosis-inducing factor induced by MPP(+). Taken together, these findings reveal for the first time that Eda protects against MPP(+)-induced astrocytic apoptosis via decreasing intracellular reactive oxygen species level and subsequently inhibiting mitochondrial apoptotic pathway. The antiapoptosis effects of Eda on astrocytes may provide a new perspective on neuroprotective therapy.

Authors+Show Affiliations

Jiangsu Key Laboratory of Neurodegeneration, Department of Pharmacology, Nanjing Medical University, Nanjing, Jiangsu, China.No 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

18643790

Citation

Chen, Hui, et al. "Edaravone Protects Against MPP+ -induced Cytotoxicity in Rat Primary Cultured Astrocytes Via Inhibition of Mitochondrial Apoptotic Pathway." Journal of Neurochemistry, vol. 106, no. 6, 2008, pp. 2345-52.
Chen H, Wang S, Ding JH, et al. Edaravone protects against MPP+ -induced cytotoxicity in rat primary cultured astrocytes via inhibition of mitochondrial apoptotic pathway. J Neurochem. 2008;106(6):2345-52.
Chen, H., Wang, S., Ding, J. H., & Hu, G. (2008). Edaravone protects against MPP+ -induced cytotoxicity in rat primary cultured astrocytes via inhibition of mitochondrial apoptotic pathway. Journal of Neurochemistry, 106(6), 2345-52. https://doi.org/10.1111/j.1471-4159.2008.05573.x
Chen H, et al. Edaravone Protects Against MPP+ -induced Cytotoxicity in Rat Primary Cultured Astrocytes Via Inhibition of Mitochondrial Apoptotic Pathway. J Neurochem. 2008;106(6):2345-52. PubMed PMID: 18643790.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Edaravone protects against MPP+ -induced cytotoxicity in rat primary cultured astrocytes via inhibition of mitochondrial apoptotic pathway. AU - Chen,Hui, AU - Wang,Sen, AU - Ding,Jian-Hua, AU - Hu,Gang, Y1 - 2008/07/15/ PY - 2008/7/23/pubmed PY - 2008/11/8/medline PY - 2008/7/23/entrez SP - 2345 EP - 52 JF - Journal of neurochemistry JO - J Neurochem VL - 106 IS - 6 N2 - Edaravone (Eda) is a potent scavenger of hydroxyl radicals and has been demonstrated to be beneficial for patients with acute ischemic stroke. This study was set out to investigate whether Eda protect against MPP(+)-induced cytotoxicity in rat primary cultured astrocytes. The results showed that pre-treatment with Eda inhibited astrocytic apoptosis and lactate dehydrogenase release induced by MPP(+) (200 microM). Further study revealed that Eda prevented GSH depletion, down-regulated mRNA expressions of NADPH oxidase membrane subunit gp91 and membrane-translocated subunit p47, and prevented the decreases of state 3 respiration respiration and respiratory control ratio induced by MPP(+), and thereby inhibited reactive oxygen species production evoked by MPP(+). Moreover, Eda could ameliorate mitochondrial respiratory function, restrain, and prevent mitochondrial membrane potential loss induced by MPP(+). Consequently, Eda inhibited releases of cytochrome c and apoptosis-inducing factor induced by MPP(+). Taken together, these findings reveal for the first time that Eda protects against MPP(+)-induced astrocytic apoptosis via decreasing intracellular reactive oxygen species level and subsequently inhibiting mitochondrial apoptotic pathway. The antiapoptosis effects of Eda on astrocytes may provide a new perspective on neuroprotective therapy. SN - 1471-4159 UR - https://www.unboundmedicine.com/medline/citation/18643790/Edaravone_protects_against_MPP+__induced_cytotoxicity_in_rat_primary_cultured_astrocytes_via_inhibition_of_mitochondrial_apoptotic_pathway_ L2 - https://doi.org/10.1111/j.1471-4159.2008.05573.x DB - PRIME DP - Unbound Medicine ER -