Objective To investigate the protective effects of ATP-sensitive potassium channel (K (ATP)) opener (
Pinacidil) on cultured
cortical neurons in newborn rats after anoxic/
hypoglycemic damage. Methods Neurons were exposed to anoxic/hypoglycemic condition for 4 h,8 h,16 h, after being cultured for 10 days. All cultured neurons were divided into 4 groups: normal control group, model control group, Pinacidil (Pin) group and Pin plus Glibenclamide (Gli) group. The cell mortality, quantity of LDH and the percentage of neuron
apoptosis in each group were determined. Results Pinacidil (10~(-6)mol/L ) reduced the percentage of cell death(4 h:21.42±3.68 vs 14.83±2.94; 8 h:36.58±6.14 vs 19.25±3.33; 16 h:49.17±8.3 vs 28.64±6.4, P<0.01),percentage of released lactate dehydrogenase (LDH%)(4 h:26.9±6.1 vs 13.2±4.1; 8 h:31.4±4.9 vs 18.7±5.3; 16 h:47.7±6.5 vs 28.1±6.8, P<0.01) and neuron apoptosis(16 h: 42±7.8 vs 20.4±5.5, P<0.01). K (ATP) agonist Gli prevented the protective effects of Pin. Conclusion K (ATP) opener (Pinacidil) performs a neuroprotective role in anoxic/hypoglycemic injury which partly due to its suppression on neuron apoptosis.