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[Effect of JNK pathway in apoptosis of PC12 cell by MPP+].

AbstractOBJECTIVE:
To study the toxicity and its mechanisms of 1-methyl-4-phenylpyridinium ion (MPP+) on pheochromocytoma PC12 cells.
METHODS:
PC12 cells were cultured in vitro, and poisoned by 100, 300, 500 micromol/L MPP+. Western blot was performed to determine the level of phosphorylated c-Jun-N-terminal kinase/stress activated protein kinases (JNK/SAPK). The cells were pretreated with SP600125, an inhibitor of JNK pathway, and then the number of apoptotic cells were counted by using TUNEL stain, observing its influence on cell apoptosis seduced by MPP+.
RESULTS:
MPP+ poisoning can cause the increase of phosphorylation level of JNK1/2 cells. The usage of JNK pathway inhibitor SP600125 can inhibit the PC12 cell apoptosis seduced by MPP+.
CONCLUSION:
Activation of JNK pathway may be the important molecular mechanism of PC12 cell apoptosis seduced by MPP+ and of producing dopaminergic neurotoxicity.
AuthorsGang Zheng, Wenjing Luo, Xueping Zhang, Fang Zhao, Jiye Wang, Yaoming Chen, Jingyuan Chen
JournalWei sheng yan jiu = Journal of hygiene research (Wei Sheng Yan Jiu) Vol. 40 Issue 1 Pg. 109-11 (Jan 2011) ISSN: 1000-8020 [Print] China
PMID21434327 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Anthracenes
  • pyrazolanthrone
  • 1-Methyl-4-phenylpyridinium
Topics
  • 1-Methyl-4-phenylpyridinium (toxicity)
  • Animals
  • Anthracenes (pharmacology)
  • Apoptosis (drug effects)
  • MAP Kinase Signaling System (drug effects)
  • PC12 Cells
  • Rats

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