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Neuroprotection of Sodium Valproate against Rotenone induced Mitochondrial Dysfunction in SH-SY5Y Cells
Qiu Jing1, Gao Jing1, Xiong Yuyun2, Xia Juan1, Ma Rui3, Qian Jinjun4∗
1School of Pharmacy, Jiangsu University, Zhenjiang 212013, China; 2School of Medical Science and Laboratory Medicine, Jiangsu University, Zhenjiang 212013, China; 3School of Clinical Medicine, Jiangsu University, Zhenjiang
Abstract: To approach the effect and mitochondrial mechanism of sodium valproate (VPA) in SH-SY5Y cells， after pretreatment with different concentrations of VPA for 3 h， SH-SY5Y cells were treated with Rotenone for 24 h， which is an inhibitor of mitochondrial complex I， to induce mitochondrial dysfunction. Cell viability was analysed by MTT assay; mitochondrial membrane potential was detected by JC-1 staining and the mass of mitochondria was detected by Mito-Tracker staining; cell respiratory function was evaluated by Clark oxygen electrode; the quantity of ROS was evaluated by DCFH-DA staining; mitochondrial swelling induced by Ca2+ was also detected. We found that pretreatment of VPA for 3 h in SH-SY5Y cells could protect cells against the injury induced by 400 nmol/L Rotenone， increase mitochondrial membrane potential and elevate the mass of mitochondria， enhance the cell respiratory function and decrease the quantity of ROS. But VPA could not interact with mitochondria directly. Generally speaking， VPA has neuroprotective effect relating to enhance the function and the mass of mitochondria， against ROS generation， and recovery the function of cells subsequently.
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