中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2013年
4期
753-755
,共3页
孙忠东%宋玉娥%景丽%郑建伟
孫忠東%宋玉娥%景麗%鄭建偉
손충동%송옥아%경려%정건위
心肌保护%酸性复灌液%内质网应激%脱噬作用%再灌注损伤
心肌保護%痠性複灌液%內質網應激%脫噬作用%再灌註損傷
심기보호%산성복관액%내질망응격%탈서작용%재관주손상
Myocardial protection%Acidic reperfusion fluid%Endopasmic reticulum stress%Apoptosis%Reperfusion injury
目的 观察酸性HEPES-KH液对大鼠缺血再灌注(I/R)心肌内质网应激(ERS)与细胞凋亡的影响.方法 采用Langendorff离体灌注模型,SD大鼠24只随机分为3组(n=8):正常对照组(C),仅灌注pH 7.4 HEPES-KH液180 min;缺血/再灌组(I/R,n=8),pH 7.4 HEPES-KH液灌流20 min后缺血60 min,用pH 7.4 HEPES-KH液恢复灌注100 min；酸性复灌液组(E,n=8),pH7.4HEPES-KH液灌流20 min后缺血60 min,pH6.8和pH 7.1 HEPES-KH液依次灌注5 min,最后恢复pH 7.4 HEPES-KH液灌注90 min.以肌钙蛋白I(cTnI)浓度、心肌细胞凋亡、钙网蛋白(CRT)mRNA表达、半胱氨酰天冬氨酸特异性蛋白酶(Caspase)-12和CCAAT/增强子结合蛋白(C/EBP)同源蛋白(CHOP)表达为检测指标.结果 与C组(1.3±0.4、3.7±1.1、0.48 ±0.04、0.12 ±0.02、0.08 ±0.01)比较,I/R组和E组在cTnI浓度(12.5±3.2、6.7±1.7)、心肌细胞凋亡率[(27.9±5.3)％]、(18.0±3.9)％]、CRT mRNA(1.03±0.06、0.79 ±0.05)、Caspase-12 (0.35 ±0.05、0.24±0.03)和CHOP(0.19 ±0.04、0.13 ±0.03)蛋白表达均明显增加(P＜0.01)；E组与I/R组比较,各检测指标均降低(P＜0.01).结论 再灌注初短暂酸性梯度复灌液可调控ERS反应程度,抑制I/R导致的过度ERS介导的细胞凋亡的发生,从而产生心肌保护作用.
目的 觀察痠性HEPES-KH液對大鼠缺血再灌註(I/R)心肌內質網應激(ERS)與細胞凋亡的影響.方法 採用Langendorff離體灌註模型,SD大鼠24隻隨機分為3組(n=8):正常對照組(C),僅灌註pH 7.4 HEPES-KH液180 min;缺血/再灌組(I/R,n=8),pH 7.4 HEPES-KH液灌流20 min後缺血60 min,用pH 7.4 HEPES-KH液恢複灌註100 min；痠性複灌液組(E,n=8),pH7.4HEPES-KH液灌流20 min後缺血60 min,pH6.8和pH 7.1 HEPES-KH液依次灌註5 min,最後恢複pH 7.4 HEPES-KH液灌註90 min.以肌鈣蛋白I(cTnI)濃度、心肌細胞凋亡、鈣網蛋白(CRT)mRNA錶達、半胱氨酰天鼕氨痠特異性蛋白酶(Caspase)-12和CCAAT/增彊子結閤蛋白(C/EBP)同源蛋白(CHOP)錶達為檢測指標.結果 與C組(1.3±0.4、3.7±1.1、0.48 ±0.04、0.12 ±0.02、0.08 ±0.01)比較,I/R組和E組在cTnI濃度(12.5±3.2、6.7±1.7)、心肌細胞凋亡率[(27.9±5.3)％]、(18.0±3.9)％]、CRT mRNA(1.03±0.06、0.79 ±0.05)、Caspase-12 (0.35 ±0.05、0.24±0.03)和CHOP(0.19 ±0.04、0.13 ±0.03)蛋白錶達均明顯增加(P＜0.01)；E組與I/R組比較,各檢測指標均降低(P＜0.01).結論 再灌註初短暫痠性梯度複灌液可調控ERS反應程度,抑製I/R導緻的過度ERS介導的細胞凋亡的髮生,從而產生心肌保護作用.
목적 관찰산성HEPES-KH액대대서결혈재관주(I/R)심기내질망응격(ERS)여세포조망적영향.방법 채용Langendorff리체관주모형,SD대서24지수궤분위3조(n=8):정상대조조(C),부관주pH 7.4 HEPES-KH액180 min;결혈/재관조(I/R,n=8),pH 7.4 HEPES-KH액관류20 min후결혈60 min,용pH 7.4 HEPES-KH액회복관주100 min；산성복관액조(E,n=8),pH7.4HEPES-KH액관류20 min후결혈60 min,pH6.8화pH 7.1 HEPES-KH액의차관주5 min,최후회복pH 7.4 HEPES-KH액관주90 min.이기개단백I(cTnI)농도、심기세포조망、개망단백(CRT)mRNA표체、반광안선천동안산특이성단백매(Caspase)-12화CCAAT/증강자결합단백(C/EBP)동원단백(CHOP)표체위검측지표.결과 여C조(1.3±0.4、3.7±1.1、0.48 ±0.04、0.12 ±0.02、0.08 ±0.01)비교,I/R조화E조재cTnI농도(12.5±3.2、6.7±1.7)、심기세포조망솔[(27.9±5.3)％]、(18.0±3.9)％]、CRT mRNA(1.03±0.06、0.79 ±0.05)、Caspase-12 (0.35 ±0.05、0.24±0.03)화CHOP(0.19 ±0.04、0.13 ±0.03)단백표체균명현증가(P＜0.01)；E조여I/R조비교,각검측지표균강저(P＜0.01).결론 재관주초단잠산성제도복관액가조공ERS반응정도,억제I/R도치적과도ERS개도적세포조망적발생,종이산생심기보호작용.
Objective To determine the effect of acidic reperfusion solution on apoptosis of myocardial endoplasmic reticulum stress (ERS).Methods Twenty-four SD rats were randomly divided into 3 groups (n =8 each).In control group (C),the isolated heart was only reperfused 180 min with pH 7.4 HEPES-KH solution.In ischemia/reperfusion (I/R) group,the isolated heart was reperfused 20 min and then subjected to ischemia for 60 min followed by 100 min reperfusion with pH 7.4 HEPES-KH solution.In experiment group (E),the isolated heart was reperfused 20 min with pH 7.4 HEPES-KH solution and then subjected to ischemia for 60 min,followed by reperfusion with pH6.8,pH 7.1 and pH 7.4 HEPES-KH solution for 5 min,5 min,and 90 min,respectively.Cardiac troponin I (cTnI) concentration,apoptosis of myocardial cells,the expression levels of calreticulin (CRT) mRNA,the expression levels of Caspase-12 and CCAAT/enhancer binding protein (C/EBP) homologous protein (CHOP) were assayed.Results As compared with C group (1.3 ±0.4,3.7 ± 1.1,0.48 ±0.04,0.12 ±0.02,0.08 ±0.01),in I/R group and E group,the cTnI concentration (12.5 ±3.2,6.7 ± 1.7),apoptosis rate (27.9 ±5.3,18.0 ± 3.9),expressions of CRT mRNA (1.03 ± 0.06,0.79 ± 0.05),Caspase-12 (0.35 ± 0.05,0.24 ± 0.03) and CHOP (0.19 ±0.04,0.13 ±0.03) were increased significantly (P ＜0.01).All the indexes in E group were significantly reduced as compared with I/R group (P ＜0.01).Conclusion Acidic reperfusion may protect the heart against I/R injury and alleviate ERS-mediated apoptosis by inhibiting excessive ERS during I/R.
