Oxidative Medicine and Cellular Longevity / 2020 / Article / Fig 5

Research Article

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

Figure 5

Sal enhanced mitophagy after SCIRI. (a) Electron micrographs demonstrating neuron mitophagy structure in Sal-treated SCIRI mice. Typical mitophagy structure (white arrow) was observed in neurons. The high magnifications of lower box revealed a typical structure of (A) normal mitochondria, (B) swollen mitochondria, (C) autolysosomes, and (D) mitophagy from the four groups of mice mentioned above. Scale bar, 0.5 μm. (b) Immunohistochemical colocalization of Tomm20 (mitochondrial marker, green) and LAMP2 (lysosomal marker, red) in the spinal cords from the four groups of mice mentioned above at 12 h after SCIRI. The inset images represent higher magnification of the boxed area in the corresponding merged images. Scale bar, 100 μm. (c) Quantification of the ratio of mitochondria engulfed by autophagosomes to total mitochondria in each field. (d) Statistical analysis of the ratio of LAMP2-associated Tomm20 to total Tomm20. (e) Representative images of mt-Keima to detect normal mitochondria (in green) and mitochondria in autophagosomes (in red), in neurons. Neurons were treated with DMSO, different concentrations of Sal, with or without OGD/R for 12 h. Scale bar, 100 μm. (f) Quantification of the ratio of red to green dots in neurons. Representative (g) western blots and (h–j) quantitative graphs demonstrated the expression of LC3-B, P62, and Tomm20 in whole homogenates normalized to the level of β-actin. All values are presented as (); , , and .

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