Squamosamide Derivative FLZ Protects Pancreatic β-Cells from Glucotoxicity by Stimulating Akt-FOXO1 Pathway

Figure 3

FLZ restores glucotoxicity-altered expression and intracellular localization of PDX-1 and FOXO1. ((a), (c)) INS-1E cells were cultured at G5.5 or G30 for 3 days. Cells were treated without or with 10 μM FLZ. Expression of PDX-1 (a) or pFOXO1 (c) protein was determined by western blot. β-actin was used as an internal control ((a), upper panel). Intensities of PDX-1 (a) or pFOXO1 (c) protein expression were quantified, normalized against the level of β-actin (a) or total FOXO1 (c), and expressed as fold of protein abundance in INS-1E cells at G5.5 (low panels). Data are means ± S.E.M. of 3 separate experiments each. versus the value at G5.5; versus the value at G30 without FLZ. ((b), (d)) INS-1E cells were cultured at G5.5 or G30 for 3 days. Cells were treated without or with 10 μM FLZ. Nuclear protein extraction was subjected to western blot analysis. Lamin B was used as an internal control (upper panels). Intensities of PDX-1 (b) or FOXO1 (d) protein expression were quantified, normalized against the level of Lamin B, and expressed as fold of protein abundance in INS-1E cells at G5.5 (low panels). Means ± S.E.M. results of 3 separate experiments each. , versus the value at G5.5; versus the value at G30 without FLZ.

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