Journal: PPAR Research
Article Title: HDAC Inhibition Modulates Cardiac PPARs and Fatty Acid Metabolism in Diabetic Cardiomyopathy
doi: 10.1155/2016/5938740
Figure Lengend Snippet: Cardiac fatty acid metabolic proteins in control, diabetes mellitus (DM), and MPT0E014-treated DM (DM + MPT0E014) rats. Representative immunoblots and average data of (a) ratio of phosphorylated 5′ adenosine monophosphate-activated protein kinase 2 α (pAMPK2 α ) to total AMPK2 α , (b) peroxisome proliferator-activated receptor- (PPAR-) γ coactivator- (PGC-) 1 α , (c) phosphorylated acetyl coenzyme A carboxylase (pACC), (d) cluster of differentiation 36 (CD36), (e) diacylglycerol acyltransferase 1 (DGAT1), and (f) DGAT2 from control ( n = 4), DM ( n = 4), and DM + MPT0E014 ( n = 4) rats. Densitometry was normalized to glyceraldehyde 3-phosphate dehydrogenase (GAPDH) as an internal control.
Article Snippet: Blots were probed with antibodies against PPAR- α (Santa Cruz Biotechnology, Santa Cruz, CA, USA), PPAR- γ (Santa Cruz Biotechnology), PPAR- δ (Affinity Bio Reagent, Golden, CO, USA), tumor necrosis factor- (TNF-) α (AbDSerotec, MorphoSys UK, Oxford, UK), interleukin- (IL-) 6 (Bender MedSystems, Vienna, Austria), PPAR- γ coactivator- (PGC-) 1 α (Abcam, Cambridge, UK), 5′ adenosine monophosphate-activated protein kinase 2 α (AMPK2 α ) (Cell Signaling, Beverly, MA, USA), phosphorylated acetyl coenzyme A carboxylase (pACC) (Millipore, St. Louis, MO, USA), diacylglycerol acyltransferase 1 (DGAT1) (Abcam), DGAT2 (Abcam), cluster of differentiation 36 (CD36) (Abcam), phosphorylated AMPK2 α (pAMPK2 α ) (Millipore), Akt (Cell Signaling), phosphorylated Akt (pAkt) (Cell Signaling), and secondary antibodies conjugated with horseradish peroxidase (HRP; Leinco Technology, St. Louis, MO, USA).
Techniques: Western Blot
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