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Effects of edaravone on high glucose-induced apoptosis in SH-SY5 Y cells via regulating microRNA-25 / 中国病理生理杂志
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-509068
Responsible library: WPRO
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.

Full text: Available Database: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2017 Document type: Article
Full text: Available Database: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2017 Document type: Article
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