Oxidative Medicine and Cellular Longevity / 2020 / Article / Fig 7

Research Article

SOCS2 Inhibits Mitochondrial Fatty Acid Oxidation via Suppressing LepR/JAK2/AMPK Signaling Pathway in Mouse Adipocytes

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 (). (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 (). (c) SOCS2 mRNA expression levels after transfection with Ad-SOCS2 and sh-SOCS2 and 10 μM coumermycin A1 treatment for 30 min (). (d) Leptin receptor mRNA level after transfection with Ad-SOCS2 and sh-SOCS2 and 10 μM coumermycin A1 treatment for 30 min (). (e–g) Protein levels of p-ACC, CPT-1b, and FABP4 after transfection with SOCS2 and 10 μM coumermycin A1 treatment for 30 min (). (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 (). (i) p-AMPK level after transfection with SOCS2 and 10 μM coumermycin A1 treatment for 30 min (). All the protein levels (a, e–g, i) were detected by the ELISA test. Values are the . , .
(a)
(b)
(c)
(d)
(e)
(f)
(g)
(h)
(i)

Article of the Year Award: Outstanding research contributions of 2020, as selected by our Chief Editors. Read the winning articles.