Research Article

Cardiomyocyte-Restricted Deletion of PPARβ/δ in PPARα-Null Mice Causes Impaired Mitochondrial Biogenesis and Defense, but No Further Depression of Myocardial Fatty Acid Oxidation

Figure 5

Endogenous anti oxidants and oxidative stress. (a) Real-time PCR analysis of transcript expression of SOD1, SOD2, and catalase on samples from TMCM, PPARα −/−, TMPD, and TMPDPA hearts. (b, c, and d) Western blotting analysis of protein levels of SOD1, SOD2, and catalase on samples from TMCM, PPARα −/−, TMPD, and TMPDPA hearts. (e) Mitochondrial membrane potential estimated by JC-1 uptake assay in isolated mitochondria from TMCM, PPARα −/−, TMPD, and TMPDPA hearts. (f) Mitochondrial aconitase activity of samples from TMCM, PPARα −/−, TMPD, and TMPDPA hearts. 𝑃 < 0 . 0 5 versus TMCM; 𝑃 < 0 . 0 1 versus TMCM.
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