Salidroside Ameliorates Mitochondria-Dependent Neuronal Apoptosis after Spinal Cord Ischemia-Reperfusion Injury Partially through Inhibiting Oxidative Stress and Promoting Mitophagy

Figure 6

Sal promoted mitophagy via modulating the PINK1-Parkin signaling pathway. Representative western blots of the expression of mitochondrial proteins (Parkin and PINK1) in the (a) neurons and (b) spinal cords that were subjected to OGD/R or I/R for 12 h, respectively. (c–f) Quantification of Parkin and PINK1 protein expression normalized to the level of VDAC. Representative (g) confocal images and (h) statistical analysis of the colocalization of Parkin with mitochondrial neurons. The neurons were treated with DMSO and different concentrations of Sal, with or without OGD/R for 12 h. Scale bar, 100 μm. (i, k) Representative images of immunofluorescent labeling of p-Parkin (i), p-ubiquitin (k, in green), NeuN (in red), and DAPI (in blue) in the spinal cords of mice that underwent sham operation or ischemia-reperfusion injury for 12 h. Scale bars, 200 μm. Statistical analysis based on the expression of (j) p-Parkin and (l) p-ubiquitin from mice in the sham group. All values are presented as (); , , and .