中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2014年
2期
350-352
,共3页
文冰%焦周阳%付国伟%刘超%舒礼良%赵文增
文冰%焦週暘%付國偉%劉超%舒禮良%趙文增
문빙%초주양%부국위%류초%서례량%조문증
Caspase-3抑制剂%体外循环%肌酸激酶同工酶%肌钙蛋白Ⅰ%Caspase-3活性%髓过氧化物酶
Caspase-3抑製劑%體外循環%肌痠激酶同工酶%肌鈣蛋白Ⅰ%Caspase-3活性%髓過氧化物酶
Caspase-3억제제%체외순배%기산격매동공매%기개단백Ⅰ%Caspase-3활성%수과양화물매
The Caspase-3 inhibitor%Cardiopulmonary bypass%Creatine kinase isoenzyme MB%Cardiac troponin Ⅰ%Caspase-3 activity%Myeloperoxidase
目的 观察半胱氨酰天冬氨酸特异性蛋白酶(Caspase)-3抑制剂对体外循环时心肌的保护作用.方法 清洁健康新西兰大白兔(体质量为2.0 ～2.5 kg,雌雄不拘)30只,随机分为对照组和Caspase-3抑制剂Ac-DEVD-CHO组(术前0.5h经股静脉给予Ac-DEVD-CHO 5 ml/kg,术中停止体外循环后再经股静脉给予5 ml/kg).分别在术前、体外循环转流中和转流后检测各组肌酸激酶同工酶(CK-MB)、心肌肌钙蛋白(cTnⅠ)、Caspase-3活性和髓过氧化物酶(MPO)活性变化.结果 Caspase-3抑制剂组与对照组比较,血cTnⅠ水平(g/L) (0.03 ±0.02、0.03±0.06、0.08 ±0.04、0.09±0.02比0.03±0.01、0.06±0.03、0.12 ±0.05、0.17±0.07)和CK-MB浓度(U/L)均明显降低(111.39±0.03、134.26 ±3.45、342.49±5.35、501.25±8.31比100.41 ±0.02、435.21±6.38、987.32±25.17、1 264.53±22.08),Caspase-3活性(z/pmol/h/mg)受到明显抑制(0.03±0.01、0.09±0.02、0.18 ±0.03、0.39±0.02比0.02 ±0.01、0.16±0.05、0.72 ±0.04、0.87 ±0.06),MPO活性显著降低(μg/L) (0.33 ±0.02、0.53 ±0.03、0.67±0.03、0.88 ±0.05比0.33±0.01、0.96 ±0.04、1.12±0.03、2.17 ±0.02),差异有统计学意义(F=36.10 ～574.13,P＜0.05).结论 Caspase-3抑制剂对体外循环时心功能损伤起到一定的保护作用.
目的 觀察半胱氨酰天鼕氨痠特異性蛋白酶(Caspase)-3抑製劑對體外循環時心肌的保護作用.方法 清潔健康新西蘭大白兔(體質量為2.0 ～2.5 kg,雌雄不拘)30隻,隨機分為對照組和Caspase-3抑製劑Ac-DEVD-CHO組(術前0.5h經股靜脈給予Ac-DEVD-CHO 5 ml/kg,術中停止體外循環後再經股靜脈給予5 ml/kg).分彆在術前、體外循環轉流中和轉流後檢測各組肌痠激酶同工酶(CK-MB)、心肌肌鈣蛋白(cTnⅠ)、Caspase-3活性和髓過氧化物酶(MPO)活性變化.結果 Caspase-3抑製劑組與對照組比較,血cTnⅠ水平(g/L) (0.03 ±0.02、0.03±0.06、0.08 ±0.04、0.09±0.02比0.03±0.01、0.06±0.03、0.12 ±0.05、0.17±0.07)和CK-MB濃度(U/L)均明顯降低(111.39±0.03、134.26 ±3.45、342.49±5.35、501.25±8.31比100.41 ±0.02、435.21±6.38、987.32±25.17、1 264.53±22.08),Caspase-3活性(z/pmol/h/mg)受到明顯抑製(0.03±0.01、0.09±0.02、0.18 ±0.03、0.39±0.02比0.02 ±0.01、0.16±0.05、0.72 ±0.04、0.87 ±0.06),MPO活性顯著降低(μg/L) (0.33 ±0.02、0.53 ±0.03、0.67±0.03、0.88 ±0.05比0.33±0.01、0.96 ±0.04、1.12±0.03、2.17 ±0.02),差異有統計學意義(F=36.10 ～574.13,P＜0.05).結論 Caspase-3抑製劑對體外循環時心功能損傷起到一定的保護作用.
목적 관찰반광안선천동안산특이성단백매(Caspase)-3억제제대체외순배시심기적보호작용.방법 청길건강신서란대백토(체질량위2.0 ～2.5 kg,자웅불구)30지,수궤분위대조조화Caspase-3억제제Ac-DEVD-CHO조(술전0.5h경고정맥급여Ac-DEVD-CHO 5 ml/kg,술중정지체외순배후재경고정맥급여5 ml/kg).분별재술전、체외순배전류중화전류후검측각조기산격매동공매(CK-MB)、심기기개단백(cTnⅠ)、Caspase-3활성화수과양화물매(MPO)활성변화.결과 Caspase-3억제제조여대조조비교,혈cTnⅠ수평(g/L) (0.03 ±0.02、0.03±0.06、0.08 ±0.04、0.09±0.02비0.03±0.01、0.06±0.03、0.12 ±0.05、0.17±0.07)화CK-MB농도(U/L)균명현강저(111.39±0.03、134.26 ±3.45、342.49±5.35、501.25±8.31비100.41 ±0.02、435.21±6.38、987.32±25.17、1 264.53±22.08),Caspase-3활성(z/pmol/h/mg)수도명현억제(0.03±0.01、0.09±0.02、0.18 ±0.03、0.39±0.02비0.02 ±0.01、0.16±0.05、0.72 ±0.04、0.87 ±0.06),MPO활성현저강저(μg/L) (0.33 ±0.02、0.53 ±0.03、0.67±0.03、0.88 ±0.05비0.33±0.01、0.96 ±0.04、1.12±0.03、2.17 ±0.02),차이유통계학의의(F=36.10 ～574.13,P＜0.05).결론 Caspase-3억제제대체외순배시심공능손상기도일정적보호작용.
Objective To investigate the protection of the Caspase-3 inhibitor (Ac-DEVD-CHO) on cardiopulmonary bypass (CPB)-induced ischemia reperfusion injury in the rabbit model.Methods Rabbits were divided into two groups:control (C) group and Ac-DEVD-CHO (A) group.In the C and A groups,animals underwent CPB at a flow rate of 50-70 ml/kg per min,Ac-DEVD-CHO (5 ml/kg) was administered to the A group rabbits by intravenous injection 30 min before operation and Ac-DEVD-CHO (5 ml/kg) was administered by intravenous infusion while reperfusion being done.The myeloperoxidase (MPO) and Caspase-3 activity,the blood creatine kinase isoenzyme MB (CK-MB) and cardiac troponin Ⅰ (cTnⅠ) in each group were detected.Results A comparison between A group and C group showed that for treated group,the levels of CK-MB (U/L) (111.39 ± 0.03,134.26 ± 3.45,342.49 ± 5.35,501.25 ±8.31 vs.100.41 ± 0.02,435.21 ± 6.38,987.32 ± 25.17,1 264.53 ± 22.08) and cTnⅠ (g/L) (0.03 ±0.02,0.03±0.06,0.08±0.04,0.09±0.02 vs.0.03 ±0.01,0.06±0.03,0.12±0.05,0.17±0.07)were both decreased,the activity of Caspase-3 (z/pmol/h/mg) (0.03 ±0.01,0.09 ±0.02,0.18 ±0.03,0.39±0.02 vs.0.02±0.01,0.16 ±0.05,0.72 ±0.04,0.87 ±0.06) and MPO(μg/L) (0.33±0.02,0.53 ±0.03,0.67 ±0.03,0.88 ±0.05 vs.0.33 ± 0.01,0.96 ±0.04,1.12 ±0.03,2.17 ±0.02) were inhibited (F =36.10-574.13,P ＜ 0.05).The differences of the above items were of statistically significant.Conclusion Ac-DEVD-CHO inhibited the changes in the MPO and Caspase-3 activity and decreased the blood CK-MB and cTnⅠ in simulated extracorporeal circulation.This study suggests that Ac-DEVD-CHO could be feasible therapeutic strategy to protect the cardiac function injury in patients undergoing cardiopulmonary bypass.
