药学学报
藥學學報
약학학보
ACTA PHARMACEUTICA SINICA
2005年
7期
644-648
,共5页
董德利%宋维华%马培林%杨宝峰
董德利%宋維華%馬培林%楊寶峰
동덕리%송유화%마배림%양보봉
三氧化二砷%HeLa细胞%电压依赖性钾电流%四氨基吡啶%四乙基铵
三氧化二砷%HeLa細胞%電壓依賴性鉀電流%四氨基吡啶%四乙基銨
삼양화이신%HeLa세포%전압의뢰성갑전류%사안기필정%사을기안
arsenic trioxide%HeLa cells%voltage-dependent K + currents%4-aminopyridine%tetraethylammonium
目的研究钾通道阻滞剂对三氧化二砷诱导的HeLa细胞死亡的作用.方法采用MTT法评价HeLa细胞的存活情况,采用膜片钳技术记录HeLa细胞的电压依赖性钾电流.结果As2O3(5 μmol·L-1)孵育24 h引起显著的HeLa细胞死亡,As2O3(5μmol·L-1)孵育24 h后存活的细胞表现明显的电压依赖性钾电流密度增加.+80mV电压下,As2O3(5 μmol·L-1)孵育组电流密度(61±18)pA/10pF(n=8)明显高于对照组(38±10)pA/10pF(n=8,P＜0.05).As2O3诱导的HeLa细胞死亡可被共同孵育钾通道阻滞剂四氨基吡啶(3 mmol·L-1)或四乙基铵(5 mmol·L-1)所部分抑制.3 mmol·L-1四氨基吡啶或5 mmol·L-1四乙基铵对HeLa细胞无明显细胞毒作用.结论As2O3长期处理增加HeLa细胞的电压依赖性钾电流.As2O3诱导的HeLa细胞死亡可被钾通道阻滞剂四氨基吡啶或四乙基铵部分抑制.
目的研究鉀通道阻滯劑對三氧化二砷誘導的HeLa細胞死亡的作用.方法採用MTT法評價HeLa細胞的存活情況,採用膜片鉗技術記錄HeLa細胞的電壓依賴性鉀電流.結果As2O3(5 μmol·L-1)孵育24 h引起顯著的HeLa細胞死亡,As2O3(5μmol·L-1)孵育24 h後存活的細胞錶現明顯的電壓依賴性鉀電流密度增加.+80mV電壓下,As2O3(5 μmol·L-1)孵育組電流密度(61±18)pA/10pF(n=8)明顯高于對照組(38±10)pA/10pF(n=8,P＜0.05).As2O3誘導的HeLa細胞死亡可被共同孵育鉀通道阻滯劑四氨基吡啶(3 mmol·L-1)或四乙基銨(5 mmol·L-1)所部分抑製.3 mmol·L-1四氨基吡啶或5 mmol·L-1四乙基銨對HeLa細胞無明顯細胞毒作用.結論As2O3長期處理增加HeLa細胞的電壓依賴性鉀電流.As2O3誘導的HeLa細胞死亡可被鉀通道阻滯劑四氨基吡啶或四乙基銨部分抑製.
목적연구갑통도조체제대삼양화이신유도적HeLa세포사망적작용.방법채용MTT법평개HeLa세포적존활정황,채용막편겸기술기록HeLa세포적전압의뢰성갑전류.결과As2O3(5 μmol·L-1)부육24 h인기현저적HeLa세포사망,As2O3(5μmol·L-1)부육24 h후존활적세포표현명현적전압의뢰성갑전류밀도증가.+80mV전압하,As2O3(5 μmol·L-1)부육조전류밀도(61±18)pA/10pF(n=8)명현고우대조조(38±10)pA/10pF(n=8,P＜0.05).As2O3유도적HeLa세포사망가피공동부육갑통도조체제사안기필정(3 mmol·L-1)혹사을기안(5 mmol·L-1)소부분억제.3 mmol·L-1사안기필정혹5 mmol·L-1사을기안대HeLa세포무명현세포독작용.결론As2O3장기처리증가HeLa세포적전압의뢰성갑전류.As2O3유도적HeLa세포사망가피갑통도조체제사안기필정혹사을기안부분억제.
Aim To investigate the effects of K + channel blockers on arsenic trioxide-induced HeLa cell death. Methods Viability of HeLa cells was assessed by mitochondrial dehydrogenase activity using colorimetric MTT assay and the voltage-dependent K+ currents were recorded by using patch-clamp rest living cells after As2 O3 24 h-incubation showed significant increase of K + currents densities. At + 80mV, the densities of K+ currents (61 ± 18) pA/10 pF (n = 8) in As2O3 24 h-incubation group were significantly more than that in the control group (38 ± 10) pA/10 pF (n = 8, P ＜ 0. 05 ). The HeLa cells were prevented partially from As2 O3-induced cell death by co-application for 24 h with typical voltageeffects on HeLa cells. Conclusion Chronic treatment with As2 O3 increased voltage-dependent K+currents in HeLa cells and the cell death induced by As2O3 was reduced partially by voltage-dependent K +channel blockers, 4-aminopyridine or tetraethylammonium.
