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<0.01 vs 11.1 G, P<0.01 vs 16.7 G) and inhibited KV currents at 40 mV (45.73±15.34 pA/pF for oxymatrine, 73.80±19.23 pA/pF for control, P<0.05). After the INS-1 cells were treated with oxymatrine for 12 and 24 hr, KV2.1 channel protein was up-regulated (P<0.01 vs Control). At the same time, compared with the high glucose and high fat group, cell viability and proliferation ability were increased (P<0.01). The cell apoptotic rate was reduced, reaching 17.30%±1.00% at 12 hr and 10.35%±1.52% at 24 hr (P<0.01). These protective effects of oxymatrine were reversed by using Stromatoxin-1, a kv channel inhibitor.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.