期刊
EUROPEAN JOURNAL OF PHARMACOLOGY
卷 786, 期 -, 页码 53-59出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2016.05.031
关键词
Icaritin; 1-Methyl-4-phenylpyridinium ion; Insulin-like growth factor-1 receptor; Akt; ERK1/2; MES23.5 cells
资金
- National Natural Science Foundation of China [30971004, 31271150, 81430024]
- Taishan Scholars Construction Project, Shandong
Icaritin, a natural derivative of Icariin, is the major bioactive component of Epimedium Genus. The present study tested the hypothesis that the neuroprotective effects of Icaritin against 1-Methyl-4-phenylpyridinium ion (MPP+)-induced toxicity involved activation of the insulin-like growth factor-1 receptor (IGF-1R) signaling pathway in MES23.5 cells. Our results revealed that Icaritin pretreatment attenuated the MPP-induced decrease of cell viability in a dose-dependent fashion. Co-pretreatment with phosphatidylinositol 3-kinase (PI3-K) inhibitor LY294002, mitogen-activated protein kinase (MEK) inhibitor PD98059 or IGF-1 receptor antagonist JB-1 could completely block the protective effects of Icaritin. Moreover, Icaritin pretreatment down -regulated MPP+-induced increase of Bax/Bcl-2 ratio transcriptionally and post-transcriptionally. Further study revealed that Icaritin pretreatment could restore the decreased protein expression of Akt and extracellular signal -regulated kinase 1/2 (ERK1/2) induced by MPP+ and these effects could be completely abolished by LY294002, PD98059 or JB-1. Additionally, Icaritin treatment alone time -dependently enhanced the phosphorylation of Akt and ERK1/2 in MES23.5 cells. The activation of Akt and ERK1/2 by Icaritin could be completely blocked by JB-1, LY294002 or PD98059. Taken together, our data demonstrate that IGF-1 receptor mediated activation of PI3K/Akt and MEK/ERK1/2 signaling pathways are involved in the protective effects of Icaritin against MPP+-induced toxicity in MES23.5 cells. (C) 2016 Elsevier B.V. All rights reserved.
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