Figure 3: MK801 attenuated the high-glucose-induced dysfunction of MIN6 β-cells. | Scientific Reports

Figure 3: MK801 attenuated the high-glucose-induced dysfunction of MIN6 β-cells.

From: An excessive increase in glutamate contributes to glucose-toxicity in β-cells via activation of pancreatic NMDA receptors in rodent diabetes

Figure 3

After glucose (16.7 mM) stimulation for 1 h, MK801 (50 μM) increased the insulin secretion (a) and Insulin mRNA expression (b) in MIN6 β-cells exposed to high glucose for 72 h. (c–d) MK801 (50 μM) increased the mRNA expression of Pdx-1 and Mafa in MIN6 β-cells exposed to high glucose for 72 h. (e) After glucose (16.7 mM) stimulation for 10 min, MK801 (50 μM) increased the intracellular ATP content of MIN6 β-cells exposed to high glucose for 72 h. (f) Representative western blot showing that MK801 reduced the cleaved caspase-3 protein in MIN6 β-cells exposed to high glucose for 72 h. (g–h) MK801 (50 μM) decreased the apoptosis of MIN6 β-cells exposed to high glucose for 72 h (n = 6, *p < 0.05 vs control, **p < 0.01 vs control, #p < 0.05 vs HG). (i) After glucose (16.7 mM) stimulation for 1 h, MK801 (50 μM) increased the insulin secretion in islets exposed to high glucose for 72 h (n = 4, *p < 0.05 vs control; #p < 0.05 vs HG.).

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