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

Figure 1

Treatment with FLZ prevents glucotoxicity in INS-1E cells. (a) INS-1E cells were cultured at G11.1 and G30 for 3–5 days and cell viability was assessed with MTT assay. Values were expressed as percentage of cell viability at G11.1. Data are means ± S.E.M. of 3–6 independent experiments. versus the value at G11.1. (b) Cell viability was assessed in INS-1E cells being cultured at G11.1 and G30 for 4 days. Cells were treated without or with varying levels of FLZ. Values were expressed as percentage of cell viability at G11.1. Data are means ± S.E.M. of 3 independent experiments. versus the value at G11.1; , versus the value at G30 without FLZ. (c) Apoptosis assessed by HO/PI staining in INS-1E cells cultured at G11.1 and G30 for 4 days. Cells were treated without or with 10 μM FLZ. Arrows indicate HO-stained cells with apoptotic bodies (upper panel). Mean values ± S.E.M. of 3 independent experiments (low panel). versus the value at G11.1; versus the value at G30 without FLZ. (d) INS-1E cells were cultured at G11.1 or G30 for 4 days. Cells were treated without or with 10 μM FLZ. Expression of total and cleaved caspase 3 protein was determined by western blot. β-actin was used as an internal control (upper panel). Intensities of total and cleaved caspase 3 protein expression were quantified, normalized against the level of β-actin, and expressed as fold of protein abundance in INS-1E cells at G11.1 (low panel). Data are means ± S.E.M. of 3 separate experiments. , versus the value at G11.1; versus the value at G30 without FLZ.

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