Figure 7.
JAK2 signaling pathway was involved in SOCS2 regulation of mitochondrial fatty acid oxidation. The mice were treated with coumermycin A1, a JAK2 signal activator, and then were treated with saline, Ad-SOCS2, and sh-SOCS2. (a) p-JAK2 levels after 10 μM coumermycin A1 treatment for 0 min, 10 min, 30 min, and 60 min (n = 4). (b) Fatty acid oxidation. Cells were treated with 10 μM coumermycin A1 for 0 min, 10 min, 30 min, and 60 min, before palmitate oxidation to CO2 was measured (n = 4). (c) SOCS2 mRNA expression levels after transfection with Ad-SOCS2 and sh-SOCS2 and 10 μM coumermycin A1 treatment for 30 min (n = 4). (d) Leptin receptor mRNA level after transfection with Ad-SOCS2 and sh-SOCS2 and 10 μM coumermycin A1 treatment for 30 min (n = 4). (e–g) Protein levels of p-ACC, CPT-1b, and FABP4 after transfection with SOCS2 and 10 μM coumermycin A1 treatment for 30 min (n = 4). (h) Fatty acid oxidation. Palmitate oxidation to CO2 was measured for 3 h after transfection with SOCS2 and 10 μM coumermycin A1 treatment for 30 min (n = 4). (i) p-AMPK level after transfection with SOCS2 and 10 μM coumermycin A1 treatment for 30 min (n = 4). All the protein levels (a, e–g, i) were detected by the ELISA test. Values are the means ± SD. ∗P < 0.05, ∗∗P < 0.01.