Fig. 6: The effects of CISD1 overexpression on mitochondrial function and neuron injury induced by OGD in vitro.
From: MiR-127-3p targeting CISD1 regulates autophagy in hypoxic–ischemic cortex

A Neurons were stained by Tuj1, ROS, Mito tracker, and TUNEL to detect the condition of neurons, the level of ROS, the condition of mitochondria and neurons apoptosis in normal group, OGD group, si-NC group, ORF-NC group, si-CISD1, and ORF-CISD1 group. Scale bar = 100 μm (Mito tracker: scale bar = 50 μm). B The bar charts of neurons viability in neurons of each group. Compared with normal group, the neurons viability decreased in OGD group. While the neurons viability increased in ORF-CISD1 group, compared with OGD group. C The level of ROS in neurons of each group. ROS significantly increased in OGD group, compared with the normal group. Whereas ROS decreased significantly in ORF-CISD1 group, compared with OGD group. D The mitochondria mean fluorescence in neurons of each group. Mito mean fluorescence significantly decreased in OGD group, compared with normal group. Whereas mito mean fluorescence significantly increased in ORF-CISD1 group, compared with OGD group. E Percentage of TUNEL/DAPI of neurons was shown in each group. TUNEL staining was used to analyze neuronal apoptosis. The percentage of TUNEL/DAPI significantly increased in OGD group, compared with normal group. Whereas percentage of TUNEL/DAPI significantly decreased in ORF-CISD1 group, compared with OGD group. The data were presented as the mean ± s.d. **P < 0.01 with one-way ANOVA, n = 6. CISD1 CDGSH iron sulfurdomain-containing protein 1, OGD oxygen glucose deprivation, HI hypoxia ischemia, ROS reactive oxygen species, ORF-CISD1 CISD1 overexpression, si-CISD1 CISD1 low expression, ORF-NC negative control overexpression, si-NC negative control low expression, Tuj1 neuronal class III β-tubulin, TUNEL terminal deoxynucleotidyl transferase dUTP nick end labeling.