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. 2020 Sep 20;9(1):576–586. doi: 10.1080/21623945.2020.1823140

Figure 3.

Figure 3.

AMPK/HO-1 contributes to the attenuation of inflammation and insulin resistance in 3T3-L1 adipocytes. (a) Western blot analysis of AMPK phosphorylation and HO-1 expression in differentiated 3T3-L1 cells treated with DEL-1 (0–1 μg/mL) for 24 h. (b) Western blot analysis of AMPK phosphorylation and HO-1 expression in AMPK or HO-1 siRNA-transfected 3T3-L1 adipocytes treated with DEL-1 (1 μg/mL) for 24 h. Western blot analysis of NFκB and IκB phosphorylation in AMPK (c) or HO-1 (d) siRNA-transfected 3T3-L1 myocytes treated with palmitate (200 μM) and DEL-1 (1 μg/mL) for 24 h. (e) ELISA for TNFα and MCP-1 release by AMPK or HO-1 siRNA-transfected 3T3-L1 adipocytes treated with DEL-1 (1 μg/mL) for 24 h. Western blot analysis of phosphorylation of IRS-1 and Akt and glucose uptake measurement (f) in AMPK or HO-1 siRNA-transfected 3T3-L1 adipocytes treated with 200 μM palmitate and DEL-1 (1 μg/mL) for 24 h. Human insulin (10 nM) stimulates insulin signalling for 3 min. Means ± SEM were obtained from three independent experiments. ***P < 0.001 when compared to control or insulin treatment. !!!P < 0.001, !!P < 0.01 and !P < 0.05 when compared to palmitate or insulin plus palmitate treatment. ###P < 0.001, ##P < 0.01 and #P < 0.05 when compared to the insulin, palmitate plus DEL-1 or insulin, palmitate plus DEL-1 treatment