首页|Cyanidin-3-rutinoside stimulated insulin secretion through activation of L-type voltage-dependent Ca~2+ channels and the PLC-IP3 pathway in pancreatic β-cells
Cyanidin-3-rutinoside stimulated insulin secretion through activation of L-type voltage-dependent Ca~2+ channels and the PLC-IP3 pathway in pancreatic β-cells
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NSTL
Cyanidin-3-rutinoside (C3R) is an anthocyanin with anti-diabetic properties found in red-purple fruits. However, the molecular mechanisms of C3R on Ca~2+-dependent insulin secretion remains unknown. This study aimed to identify C3R's mechanisms of action in pancreatic β-cells. Rat INS-1 cells were used to elucidate the effects of C3R on insulin secretion, intracellular Ca~2+ signaling, and gene expression. The results showed that C3R at 60, 100, and 300 μM concentrations significantly increased insulin secretion via intracellular Ca~2+ signaling. The exposure of cells with C3R concentrations up to 100 μM did not affect cell viability. Pretreatment of cells with nimodipine (voltage-dependent Ca~2+ channel (VDCC) blocker), U73122 (PLC inhibitor), and 2-APB (IP3 receptor blocker) inhibited the intracellular Ca~2+ signals by C3R. Interestingly, C3R increased intracellular Ca~2+ signals and insulin secretion after depletion of endoplasmic reticulum Ca~2+ stores by thapsigargin. However, insulin secretion was abolished under extracellular Ca~2+-free conditions. Moreover, C3R upregulated mRNA expression for Glut2 and Kir6.2 genes. These findings indicate that C3R stimulated insulin secretion by promoting Ca~2+ influx via VDCCs and activating the PLC-IP3 pathway. C3R also upregulates the expression of genes necessary for glucose-induced insulin secretion. This is the first study describing the molecular mechanisms by which C3R stimulates Ca~2+-dependent insulin secretion from pancreatic β-cells. These findings contribute to our understanding on how anthocyanins improve hyperglycemia in diabetic patients.
NSTL
