Voltage-gated potassium channels are involved in oxymatrine-regulated islet function in rat islet β cells and INS-1 cells

Abstract

Objective(s): Oxymatrine can regulate glucose metabolism. But the underlying mechanisms remain unclear. We investigated the relationship of oxymatrine and voltage-gated potassium (Kv) channel in rat islet β cells and INS-1 cells.Materials and Methods: Insulin secretion and Kv channel currents were tested by radioimmunoassay and patch-clamp technique, respectively. The INS-1 cell viability was detected using cell counting kit-8 experiments. Flowcytometry analysis and western blot were employed for cell apoptosis and protein levels, respectively. INS-1 cell proliferation was assessed by the 5-Ethynyl-2’- deoxyuridine method. Results: Oxymatrine potentiated insulin secretion at high glucose (p Conclusion: The results indicate that oxymatrine can stimulate insulin secretion and decrease kv channel currents in islet β cells. Besides, oxymatrine also increases cell viability, proliferation, and reduces cell apoptosis in INS-1 cells. The effects of oxymatrine are related to kv channels. This finding provides new insight into the mechanisms of oxymatrine-regulated islet function.

Keywords

• apoptosis diabetes mellitus insulin secretion oxymatrine potassium channel voltage
• gated