Effects of edaravone on high glucose-induced apoptosis in SH-SY5 Y cells via regulating microRNA-25
10.3969/j.issn.1000-4718.2017.01.015
- VernacularTitle:依达拉奉通过microRNA－25抑制高糖诱导的SH－SY5Y细胞凋亡
- Author:
Zhenhan ZHU
;
Jie QI
- Keywords:
Edaravone;
MicroRNA-25;
High glucose;
SH-SY5Y cells;
Apoptosis
- From:
Chinese Journal of Pathophysiology
2017;33(1):92-97
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To observe the effects of edaravone on high glucose-induced apoptosis of SH-SY5Y cells and its potential mechanism .METHODS:The SH-SY5Y cells were cultured in the DMEM medium with 100 mmol/L glucose and 100μmol/L edaravone for 24 h.The viability of the SH-SY5Y cells was detected by MTT assay .The levels of ROS in the cells were determined by DCFH-DA fluorescent probing .The apoptotic rates of the cells were analyzed by flow cytome-try.The protein expression of Bax and Bcl-2 in the cells were detected by Western blot .The expression levels of micro-RNA-25 (miR-25) were determined by real-time PCR.To further clarify the target sites of edaravone on inhibiting apopto-sis induced by high glucose , miR-25 inhibitor was applied to the SH-SY5Y cells and the activity of caspase-3 was meas-ured.RESULTS:Compared with control group , the cell viability was decreased significantly in model group , and the ROS level was increased significantly .The protein expression of Bax was up-regulated significantly , while the expression levels of Bcl-2 and miR-25 were significantly down-regulated .Compared with model group , the cell viability was increased signifi-cantly in edaravone group .The ROS level was decreased significantly .Meanwhile, the expression of Bax was down-regula-ted, while the expression of Bcl-2 and miR-25 was up-regulated with statistical significance .The caspase-3 activity of the cells incubated with 100 mmol/L glucose and miR-25 inhibitor was increased .However, no alteration of caspase-3 activity with edaravone added simultaneously was observed .CONCLUSION: Edaravone inhibits the apoptosis of SH-SY5Y cells induced by high glucose with the potential target site of miR-25.
