Fig. 4: UCP2 is responsible for the Irisin-mediated beneficial effect in N2a cells. | Cell Death & Disease

Fig. 4: UCP2 is responsible for the Irisin-mediated beneficial effect in N2a cells.

From: Irisin regulates oxidative stress and mitochondrial dysfunction through the UCP2-AMPK pathway in prion diseases

Fig. 4

A–C The mRNA levels of UCP2, UCP4, and UCP5 in N2a cells after prp106–126 treatment, t test; D, E changes in UCP2 protein expression in N2a cells after prp106–126 treatment. F, G The protein expression level of UCP2 in N2a cells treated with irisin and PrP106–126. H Immunofluorescence colocalization detection of the mitochondrial markers DsRed-Mito and UCP2 in N2a cells treated with irisin and PrP106–126 (scale bar = 10 µm). I Immunofluorescence colocalization of FITC-irisin and UCP2 in N2a cells treated with irisin and PrP106–126 (scale bar = 10 µm). J Determination of N2a cell apoptosis by TUNEL staining (scale bar = 50 µm). The data are presented as the means ± SDs (n = 6), *P < 0.05; **P < 0.01; ***P < 0.001.

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