Abstract：
:Neurotoxicity is a key dose-limiting factor for colistin therapy. This study aimed to investigate the protective effect of Salidroside on colistin-induced neurotoxicity in RSC96 Schwann cells and the underlying mechanisms. After Salidroside (12.5, 25, 50 μg/mL) treatment for 2 h, the cells were cultured with 250 μg/mL colistin for 24 h. In order to investigate the role of phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) pathway, the cells were pre-treated with LY294002 (12.5 μmol/L, a specific inhibitor of PI3K phosphorylation) for 1 h before Salidroside (50 μg/mL) treatment, then were co-cultured with colistin (250 μg/mL) for 24 h. The results showed that colistin treatment could induce apoptotic cell death which was associated with oxidative stress injury. Salidroside could reduce colistin-induced neurotoxicity, decrease the effect of colistin on the reduced expression levels of p-Akt and Bcl-2, and increased the expresion of Bax, release of Cyt c, and activation of caspase-3. However, the protective effect of Salidroside against colistin-induced apoptosis was partly abolished by LY294002. These findings suggest that Salidroside could attenuate colistin-induced neurotoxicity in RSC96 Schwann cells via the PI3K/Akt pathway.
journal_name
Chem Biol Interactjournal_title
Chemico-biological interactionsauthors
Lu Z,Jiang G,Chen Y,Wang J,Muhammad I,Zhang L,Wang R,Liu F,Li R,Qian F,Li Jdoi
10.1016/j.cbi.2017.04.027subject
Has Abstractpub_date
2017-06-01 00:00:00pages
67-78eissn
0009-2797issn
1872-7786pii
S0009-2797(16)30502-6journal_volume
271pub_type
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journal_title：Chemico-biological interactions
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journal_title：Chemico-biological interactions
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