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. 2012 Aug 27;33(9):1195–1203. doi: 10.1038/aps.2012.87

Figure 2.

Figure 2

Emodin regulated adipogenesis and energy metabolism in 3T3-L1 adipocytes. (A) Emodin inhibited the adipogenesis induced by 11-DHC (an inactive glucocorticoid) but not by corticosterone (an active glucocorticoid). The values are expressed as the fold increase over the values for the dexamethasone-treated DMSO group. cP<0.01 vs DMSO-treated 11-DHC group; n=4. (B) Emodin inhibited the glycerol release induced by 10 nmol/L 11-DHC but not by 10 nmol/L corticosterone. The values are expressed as the fold increase over the values for the DMSO-treated control group. cP<0.01 vs DMSO-treated control group, fP<0.01 vs DMSO-treated 11-DHC group; n=3. (C) Emodin significantly reversed the impaired insulin-stimulated glucose uptake induced by 11-DHC but not by corticosterone. bP<0.05, cP<0.01 vs insulin-stimulated control group, fP<0.01 vs insulin stimulated 11-DHC group; n=6. (D) 11-DHC- but not corticosterone-impaired adiponectin release was reversed by 3 μmol/L of emodin in 3T3-L1 adipocytes. Values are expressed as the fold increase over the values for the DMSO-treated control group. cP<0.01 vs DMSO-treated control group, fP<0.01 vsDMSO-treated 11-DHC group; n=3.