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Aim:To investigate the role of intercellular potassium in tachyplesin-induced HL-60cells apoptosis.Methods:The concentration of intercellular potassium,cell vol-ume and mitochondrial membrane potential were examined by flow cytometry.Results:The concentration of intercellular potassium reduced in a time-depen-dent manner in tachyplesin-treated HL-60 cells.In addition,the loss of mitochon-drial membrane potential was tightly coupled with the shrinkage of cell volume.Different caspase inhibitors protected against DNA degradation but did not pre-vent the loss of HL-60 cell viability induced by tachyplesin.Ba~(2+),which was akind of blocker of volume-regulatory K~+ channels,increased the viability oftachyplesin-treated HL-60 cells and maintained mitochondrial membrane potentialand cell volume.Conclusion:Efflux of K~+ was an important reason for apoptosisin tachyplesin-treated HL-60 cells.Effiux of K~+ affected the viability of tachyplesin-treated HL-60 cells independent of the process of caspase activation.
Aim: To investigate the role of intercellular potassium in tachyplesin-induced HL-60 cells apoptosis. Methods: The concentration of intercellular potassium, cell vol-ume and mitochondrial membrane potential were examined by flow cytometry. Results: The concentration of intercellular potassium reduced in a time-dependent-dent manner in tachyplesin-treated HL-60 cells. In addition, the loss of mitochon-drial membrane potential was tightly coupled with the shrinkage of cell volume. Different caspase inhibitors protected against DNA degradation but did not pre-vent the loss of HL-60 cell viability induced by tachyplesin.Ba ~ (2 +), which was akind of blocker of volume-regulatory K ~ + channels, increased the viability of tachyplesin-treated HL-60 cells and maintained mitochondrial membrane potentialand cell volume. Conclusion: Efflux of K ~ + was an important reason for apoptosis in tachyplesin-treated HL-60 cells. Effiux of K ~ + affected the viability of tachyplesin-treated HL-60 cells independent of the process of c aspase activation.