Your privacy, your choice

We use essential cookies to make sure the site can function. We also use optional cookies for advertising, personalisation of content, usage analysis, and social media.

By accepting optional cookies, you consent to the processing of your personal data - including transfers to third parties. Some third parties are outside of the European Economic Area, with varying standards of data protection.

See our privacy policy for more information on the use of your personal data.

for further information and to change your choices.

You are viewing the site in preview mode

Skip to main content
Fig. 4 | Immunity & Ageing

Fig. 4

From: Irisin inhibits microglial senescence via TFAM-mediated mitochondrial metabolism in a mouse model of tauopathy

Fig. 4

Irisin attenuates tau-induced mitochondrial dysfunction. (A-B) Representative transmission electron (TEM) micrographs showing mitochondrial morphology in the hippocampus (Α) and the proportion of each type of mitochondria (B). Class I: mitochondria with intact cristae; Class II: swollen mitochondria with vacuolation in the cristae. Scale bar, 500 nm. N = 20 analyzed fields from 3 mice for each group. (C-D) SOD activity and MDA contents in the hippocampus. N = 5 mice for each group. (E-F) Representative TEM micrographs showing mitochondrial morphology in BV2 cells (E) and the proportion of mitochondria subclasses (F). Scale bar, 500 nm. N = 20 analyzed fields from 3 independent experiments. (G-H) Representative images (G) and quantitation (H) of TMRE and MitoSox Red fluorescence in BV2 cells. N = 6 independent experiments. Data were expressed as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001

Back to article page