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Fig. 4 | Journal of Neuroinflammation

Fig. 4

From: Microglia-derived TNF-α contributes to RVLM neuronal mitochondrial dysfunction via blocking the AMPK–Sirt3 pathway in stress-induced hypertension

Fig. 4

RVLM neuronal mitochondria were injured in SIH rats. A Representative photomicrographs of the RVLM neurons in control and SIH rats for visualization in transmission electron microscopy. Mito, mitochondria. Red arrows indicate disruption of the mitochondria with abnormal mitochondrial crests. Scale bar = 5 or 1 μm. B Representative immunoblot bands and quantitative analysis showed the expression of cytoplasmic cytochrome C (Cyt-cyto C) in the RVLM between the two groups. C Within the RVLM, AAV2:MitoEGFPmCherry infection produced punctate labeling of EGFP and mCherry, which colocalized with neuron marker NeuN. Scale bar = 20 μm. Quantitative analysis showed the degree of mitochondrial degradation by assessing the ratio value of mCherry-ONLY/total mCherry puncta. D Representative immunoblot bands and quantitative analysis showed the expression of mitochondrial respiratory chain complexes (complexes II-SDHB, III-UQCRC2, and V-ATP5A) in the RVLM of control and SIH rats. E Representative fluorescence images of reactive oxygen species (ROS) detection and statistical data of ROS production in the RVLM between the two groups. Scale bar = 100 μm. F The levels of superoxide dismutase (SOD) and catalase (CAT) were quantified by using commercial kits in each group. Data were shown as mean ± SEM and analyzed via two-tailed unpaired Student’s t-test (BF). n = 3 rats per group (B, D). n = 6 rats per group (F). n = 12 slices from 6 rats, two slices per rat (C, E). *p < 0.05, **p < 0.01, ***p < 0.001 vs. Control group

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