中国循环杂志
中國循環雜誌
중국순배잡지
CHINESE CIRCULATION JOURNAL
2009年
5期
387-390
,共4页
王耀晟%邹循锋%鲍晓明%黄晓%李萍%程晓曙
王耀晟%鄒循鋒%鮑曉明%黃曉%李萍%程曉曙
왕요성%추순봉%포효명%황효%리평%정효서
去铁敏%心肌细胞%原代培养%凋亡
去鐵敏%心肌細胞%原代培養%凋亡
거철민%심기세포%원대배양%조망
Deferoxamine%Cardiomyocyte%Primary culture%Apoptosis
目的:在心肌细胞培养液中添加去铁敏,以对抗原代培养操作过程所产生的心肌细胞损伤,并探讨其保护作用. 方法:在常规新生SD乳鼠心肌细胞原代培养液中按照不同浓度添加去铁敏.抗а-肌动蛋白免疫组化法鉴定心肌细胞.心肌细胞分为对照组(不添加去铁敏);5 μmol/L去铁敏组;15 μmol/L去铁敏组;25 μmol/L去铁敏组.MTT法检测心肌细胞存活率、乳酸脱氢酶活性检测、TUNEL法检测心肌细胞凋亡率评价各组心肌细胞的损伤程度、生存率及凋亡情况. 结果:①5μmol/L去铁敏组(69.6±5.4 IU/L)、15 μmol/L去铁敏组(35.5±3.3 IU/L)和25μmol/L去铁敏组(51.0±4.3 IU/L)的乳酸脱氢酶水平均比对照组(76.3±6.1 IU/L)低,差异均有统计学意义(P<0.05~0.01).15 μmol/L去铁敏组乳酸脱氢酶水平明显低于5 μmol/L去铁敏组和25 μmol/L去铁敏组,差异均有统计学意义(P<0.05~0.01).②15 μmol/L去铁敏组(91.28±2.57)%和25 μmol/L去铁敏组(86.03±4.66)%心肌细胞生存率均比对照组(83.13 4±5.26)%高,差异均有统计学意义(P<O.05~0.01).且15μmoL/L去铁敏组心肌细胞生存率明显高于5μmol/L去铁敏组(84.19±3.36)%和25 μmol/L去铁敏组,差异均有统计学意义(P<0.05~0.01).③5 μmol/L去铁敏组(7.11 4±0.93)、15 μmol/L去铁敏组(3.10±1.26)和25 μmol/L去铁敏组(5.03±0.82)心肌细胞凋亡指数均比对照组(8.06 4±1.51)低,差异均有统计学意义(P<0.05~0.01).15μmol/L去铁敏组心肌细胞凋亡指数低于5 μmol/L去铁敏组和25 μmol/L去铁敏组,差异均有统计学意义(P<0.05~0.01). 结论:通过在心肌细胞培养液中加入适量去铁敏,能有效对抗原代培养操作过程带来的心肌细胞损伤,起到保护作用.
目的:在心肌細胞培養液中添加去鐵敏,以對抗原代培養操作過程所產生的心肌細胞損傷,併探討其保護作用. 方法:在常規新生SD乳鼠心肌細胞原代培養液中按照不同濃度添加去鐵敏.抗а-肌動蛋白免疫組化法鑒定心肌細胞.心肌細胞分為對照組(不添加去鐵敏);5 μmol/L去鐵敏組;15 μmol/L去鐵敏組;25 μmol/L去鐵敏組.MTT法檢測心肌細胞存活率、乳痠脫氫酶活性檢測、TUNEL法檢測心肌細胞凋亡率評價各組心肌細胞的損傷程度、生存率及凋亡情況. 結果:①5μmol/L去鐵敏組(69.6±5.4 IU/L)、15 μmol/L去鐵敏組(35.5±3.3 IU/L)和25μmol/L去鐵敏組(51.0±4.3 IU/L)的乳痠脫氫酶水平均比對照組(76.3±6.1 IU/L)低,差異均有統計學意義(P<0.05~0.01).15 μmol/L去鐵敏組乳痠脫氫酶水平明顯低于5 μmol/L去鐵敏組和25 μmol/L去鐵敏組,差異均有統計學意義(P<0.05~0.01).②15 μmol/L去鐵敏組(91.28±2.57)%和25 μmol/L去鐵敏組(86.03±4.66)%心肌細胞生存率均比對照組(83.13 4±5.26)%高,差異均有統計學意義(P<O.05~0.01).且15μmoL/L去鐵敏組心肌細胞生存率明顯高于5μmol/L去鐵敏組(84.19±3.36)%和25 μmol/L去鐵敏組,差異均有統計學意義(P<0.05~0.01).③5 μmol/L去鐵敏組(7.11 4±0.93)、15 μmol/L去鐵敏組(3.10±1.26)和25 μmol/L去鐵敏組(5.03±0.82)心肌細胞凋亡指數均比對照組(8.06 4±1.51)低,差異均有統計學意義(P<0.05~0.01).15μmol/L去鐵敏組心肌細胞凋亡指數低于5 μmol/L去鐵敏組和25 μmol/L去鐵敏組,差異均有統計學意義(P<0.05~0.01). 結論:通過在心肌細胞培養液中加入適量去鐵敏,能有效對抗原代培養操作過程帶來的心肌細胞損傷,起到保護作用.
목적:재심기세포배양액중첨가거철민,이대항원대배양조작과정소산생적심기세포손상,병탐토기보호작용. 방법:재상규신생SD유서심기세포원대배양액중안조불동농도첨가거철민.항а-기동단백면역조화법감정심기세포.심기세포분위대조조(불첨가거철민);5 μmol/L거철민조;15 μmol/L거철민조;25 μmol/L거철민조.MTT법검측심기세포존활솔、유산탈경매활성검측、TUNEL법검측심기세포조망솔평개각조심기세포적손상정도、생존솔급조망정황. 결과:①5μmol/L거철민조(69.6±5.4 IU/L)、15 μmol/L거철민조(35.5±3.3 IU/L)화25μmol/L거철민조(51.0±4.3 IU/L)적유산탈경매수평균비대조조(76.3±6.1 IU/L)저,차이균유통계학의의(P<0.05~0.01).15 μmol/L거철민조유산탈경매수평명현저우5 μmol/L거철민조화25 μmol/L거철민조,차이균유통계학의의(P<0.05~0.01).②15 μmol/L거철민조(91.28±2.57)%화25 μmol/L거철민조(86.03±4.66)%심기세포생존솔균비대조조(83.13 4±5.26)%고,차이균유통계학의의(P<O.05~0.01).차15μmoL/L거철민조심기세포생존솔명현고우5μmol/L거철민조(84.19±3.36)%화25 μmol/L거철민조,차이균유통계학의의(P<0.05~0.01).③5 μmol/L거철민조(7.11 4±0.93)、15 μmol/L거철민조(3.10±1.26)화25 μmol/L거철민조(5.03±0.82)심기세포조망지수균비대조조(8.06 4±1.51)저,차이균유통계학의의(P<0.05~0.01).15μmol/L거철민조심기세포조망지수저우5 μmol/L거철민조화25 μmol/L거철민조,차이균유통계학의의(P<0.05~0.01). 결론:통과재심기세포배양액중가입괄량거철민,능유효대항원대배양조작과정대래적심기세포손상,기도보호작용.
Objective:To investigate the effect of adding defemxamine(DFO) in cardiomyecytes cultured medium for protecting cells a-gainst the injury from operative procedure of primary cultured cardiomyocytes in rats.Methods:Primary cultured neonatal rats'cardiomyocytes were divided into 4 groups.Control group,no DFO was added;DFO 5 tμmol/L group;DFO 15 μmol/L group and DFO 25 μmul/L group.DFO was added into the cultured medium in different and apoptosis rate were evaluated by methyl thiazolyl tetrazolium(MTT)assay,lactate dehydrogenase (LDH) activity detection and terminal deoxynucleotidyl transferase-mediated Dutp nick end labeling(TUNEL)analysis respectively. Leakage in DFO 15 μmol/L group was the lowest,35.5 4±3.3 IU/L(15 μmol/L)vs.69.6 4±5.4 IU/L(5 μmol/L)vs.51.0±er as compared with Control group(P<0.05).Survival rate in DFO 15 μmol/L group was the highest.91.28 4±2.57% in all DFO gmups were significantly reduced than that in Control group(P<0.01).Apoptosis rate in DFO 15 μmol/L group was the lowest,3.10±1.26(15μmoL/L)vs.7.11±0.93(5 μmoL/L)vs.5.03±0.82(25 μmol/L),P<0.01. Conclusion:Appropriate dose of DFO in cultured medium could effectively protect the operative injury of cardiomyocytes in primary culture procedure.