کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2530994 | 1558894 | 2016 | 7 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Involvement of IGF-1 receptor signaling pathway in the neuroprotective effects of Icaritin against MPP+-induced toxicity in MES23.5 cells Involvement of IGF-1 receptor signaling pathway in the neuroprotective effects of Icaritin against MPP+-induced toxicity in MES23.5 cells](/preview/png/2530994.png)
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.
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Journal: European Journal of Pharmacology - Volume 786, 5 September 2016, Pages 53–59