中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2008年
5期
372-375
,共4页
王晓明%曹亚南%龚卫琴%刘安恒%张卫卫%师堂旺%刘艳
王曉明%曹亞南%龔衛琴%劉安恆%張衛衛%師堂旺%劉豔
왕효명%조아남%공위금%류안항%장위위%사당왕%류염
钾通道%细胞凋亡%心肌再灌注损伤
鉀通道%細胞凋亡%心肌再灌註損傷
갑통도%세포조망%심기재관주손상
Potassium channel%Apoptosis%Myocardial reperfusion injury
目的 探讨钾离子通道在缺血再灌注(I/R)诱导心肌细胞凋亡过程中的作用.方法 在原代培养鼠心肌细胞I/R损伤诱导心肌细胞凋亡模型中,观察钾离子通道阻断剂奎宁和氯化钡对心肌细胞的存活率、半胱天门冬氨酸酶(caspase)-3活性、活性氧的活性水平和细胞膜完整性的影响.实验分为4组:(1)阴性对照组;(2)I/R阳性对照组;(3)I/R奎宁干预组;(4)I/R氯化钡干预组.结果 (1)钾离子通道阻断剂能有效抑制I/R诱导的心肌细胞凋亡,奎宁和氯化钡组细胞的成活率分别是81.1%和82.3%,与阳性对照组(52.1%)比较,差异有统计学意义(均为P＜0.01);(2)钾离子通道阻断剂能有效的抑制caspase-3活性的激活,I/R 24 h后细胞的caspase-3活性奎宁和氯化钡组分别是188.3%和191.4%,与阳性对照组(482.3%)比较,差异有统计学意义(P＜0.01);(3)钾离子通道阻断剂能有效的抑制活性氧产生,I/R 24 h后奎宁和氯化钡组在细胞内的相对活性氧活性水平分别是21.6和19.1,与阳性对照组61.4比较,活性氧活性水平降低(P＜0.01);(4)细胞膜完整性实验乳酸脱氢酶水平显示,各组I/R 96 h后细胞坏死低于10.0%.结论 在I/R诱导的心肌细胞凋亡模型中,钾离子通道阻断剂通过抑制caspase-3活性、活性氧产生介导保护心肌细胞凋亡的发生.
目的 探討鉀離子通道在缺血再灌註(I/R)誘導心肌細胞凋亡過程中的作用.方法 在原代培養鼠心肌細胞I/R損傷誘導心肌細胞凋亡模型中,觀察鉀離子通道阻斷劑奎寧和氯化鋇對心肌細胞的存活率、半胱天門鼕氨痠酶(caspase)-3活性、活性氧的活性水平和細胞膜完整性的影響.實驗分為4組:(1)陰性對照組;(2)I/R暘性對照組;(3)I/R奎寧榦預組;(4)I/R氯化鋇榦預組.結果 (1)鉀離子通道阻斷劑能有效抑製I/R誘導的心肌細胞凋亡,奎寧和氯化鋇組細胞的成活率分彆是81.1%和82.3%,與暘性對照組(52.1%)比較,差異有統計學意義(均為P＜0.01);(2)鉀離子通道阻斷劑能有效的抑製caspase-3活性的激活,I/R 24 h後細胞的caspase-3活性奎寧和氯化鋇組分彆是188.3%和191.4%,與暘性對照組(482.3%)比較,差異有統計學意義(P＜0.01);(3)鉀離子通道阻斷劑能有效的抑製活性氧產生,I/R 24 h後奎寧和氯化鋇組在細胞內的相對活性氧活性水平分彆是21.6和19.1,與暘性對照組61.4比較,活性氧活性水平降低(P＜0.01);(4)細胞膜完整性實驗乳痠脫氫酶水平顯示,各組I/R 96 h後細胞壞死低于10.0%.結論 在I/R誘導的心肌細胞凋亡模型中,鉀離子通道阻斷劑通過抑製caspase-3活性、活性氧產生介導保護心肌細胞凋亡的髮生.
목적 탐토갑리자통도재결혈재관주(I/R)유도심기세포조망과정중적작용.방법 재원대배양서심기세포I/R손상유도심기세포조망모형중,관찰갑리자통도조단제규저화록화패대심기세포적존활솔、반광천문동안산매(caspase)-3활성、활성양적활성수평화세포막완정성적영향.실험분위4조:(1)음성대조조;(2)I/R양성대조조;(3)I/R규저간예조;(4)I/R록화패간예조.결과 (1)갑리자통도조단제능유효억제I/R유도적심기세포조망,규저화록화패조세포적성활솔분별시81.1%화82.3%,여양성대조조(52.1%)비교,차이유통계학의의(균위P＜0.01);(2)갑리자통도조단제능유효적억제caspase-3활성적격활,I/R 24 h후세포적caspase-3활성규저화록화패조분별시188.3%화191.4%,여양성대조조(482.3%)비교,차이유통계학의의(P＜0.01);(3)갑리자통도조단제능유효적억제활성양산생,I/R 24 h후규저화록화패조재세포내적상대활성양활성수평분별시21.6화19.1,여양성대조조61.4비교,활성양활성수평강저(P＜0.01);(4)세포막완정성실험유산탈경매수평현시,각조I/R 96 h후세포배사저우10.0%.결론 재I/R유도적심기세포조망모형중,갑리자통도조단제통과억제caspase-3활성、활성양산생개도보호심기세포조망적발생.
Objective To explore the role of potassium channel in cardiomyocyte apoptosis induced by ischemia/reperfusion process. Methods Cell viability,caspase-3 activity,intracellular reactive oxygen species(ROS)levels and cell membrane integrity were observed in apoptotic model of mouse cardiomyocytes induced by ischemia/reperfusion(I/R).Experiment groups included negative control,positive control(I/R)and drug treatment group(I/R + potassium channel blocker).Results (1)Potassium channel blockers potently inhibited cardiomyocyte apoptosis induced by I/R.Cell viability in Quinine(81.1%)and BaCl2(82.3%)groups were higher than in positive group (52.1%)(all P＜0.01).(2)Compared with positive control group(482.3%),potassium channel blockers(188.3% in Quinine group and 191.4% in BaCl2 group)inhibited caspase-3 activity significantly 24 hours after reperfusion(P＜0.01).(3)In both positive control and drug groups,the cell lactate dehydrogenase(LDH)leakage was less than 10% at 96 hours after reperfusion.Conclusions Potassium channel blockers can protect injured cardiomyocyte by inhibiting caspase-3 activity and ROS production in I/R process.
