中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2013年
3期
557-559
,共3页
孙忠东%郑建伟%宋玉娥%马海峰
孫忠東%鄭建偉%宋玉娥%馬海峰
손충동%정건위%송옥아%마해봉
酸性复灌液%葡萄糖调节蛋白78%内质网应激
痠性複灌液%葡萄糖調節蛋白78%內質網應激
산성복관액%포도당조절단백78%내질망응격
Acidic reperfusion fluid%Glucose-regulated protein 78%Endopasmic reticulum stress
目的 观察酸性复灌液对大鼠缺血再灌注(I/R)心肌内质网应激(ERS)葡萄糖调节蛋白78 (GRP78)的影响.方法 采用Langendorff离体心脏灌注模型,SD大鼠24只随机分为3组(n=8):正常对照组(C),灌注pH 7.4 HEPES-KH液180 min；缺血/再灌组(I/R,n=8),pH 7.4HEPES-KH液灌流20 min后缺血60 min,pH 7.4 HEPES-KH液恢复灌注100 min；酸性复灌液组(E,n=8),pH 7.4 HEPES-KH液灌流20 min后缺血60 min,复灌初先用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、GRP78 mRNA和蛋白表达为检测指标.结果 与C组[1.3±0.4、(3.7±1.1)％、0.43 ±0.04、384±75]比较,I/R组和E组在肌钙蛋白Ⅰ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)％]、GRP78 mRNA表达(0.95±0.07、0.62±0.06)和GRP78蛋白(769±132、542±98)表达均明显增加(P＜0.01)；E组与I/R组比较,cTnI浓度、心肌细胞凋亡率、GRP78 mRNA和GRP78蛋白表达均降低(P＜0.01).结论 再灌注初期短暂酸性复灌液可调节GRP78的表达,调控ERS反应程度,减轻内质网凋亡信号介导的细胞凋亡发生,从而产生心肌保护作用.
目的 觀察痠性複灌液對大鼠缺血再灌註(I/R)心肌內質網應激(ERS)葡萄糖調節蛋白78 (GRP78)的影響.方法 採用Langendorff離體心髒灌註模型,SD大鼠24隻隨機分為3組(n=8):正常對照組(C),灌註pH 7.4 HEPES-KH液180 min；缺血/再灌組(I/R,n=8),pH 7.4HEPES-KH液灌流20 min後缺血60 min,pH 7.4 HEPES-KH液恢複灌註100 min；痠性複灌液組(E,n=8),pH 7.4 HEPES-KH液灌流20 min後缺血60 min,複灌初先用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、GRP78 mRNA和蛋白錶達為檢測指標.結果 與C組[1.3±0.4、(3.7±1.1)％、0.43 ±0.04、384±75]比較,I/R組和E組在肌鈣蛋白Ⅰ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)％]、GRP78 mRNA錶達(0.95±0.07、0.62±0.06)和GRP78蛋白(769±132、542±98)錶達均明顯增加(P＜0.01)；E組與I/R組比較,cTnI濃度、心肌細胞凋亡率、GRP78 mRNA和GRP78蛋白錶達均降低(P＜0.01).結論 再灌註初期短暫痠性複灌液可調節GRP78的錶達,調控ERS反應程度,減輕內質網凋亡信號介導的細胞凋亡髮生,從而產生心肌保護作用.
목적 관찰산성복관액대대서결혈재관주(I/R)심기내질망응격(ERS)포도당조절단백78 (GRP78)적영향.방법 채용Langendorff리체심장관주모형,SD대서24지수궤분위3조(n=8):정상대조조(C),관주pH 7.4 HEPES-KH액180 min；결혈/재관조(I/R,n=8),pH 7.4HEPES-KH액관류20 min후결혈60 min,pH 7.4 HEPES-KH액회복관주100 min；산성복관액조(E,n=8),pH 7.4 HEPES-KH액관류20 min후결혈60 min,복관초선용pH6.8화pH 7.1 HEPES-KH액의차관주5 min,최후회복pH 7.4 HEPES-KH액관주90 min.이기개단백Ⅰ(cTnI)농도、심기세포조망、GRP78 mRNA화단백표체위검측지표.결과 여C조[1.3±0.4、(3.7±1.1)％、0.43 ±0.04、384±75]비교,I/R조화E조재기개단백Ⅰ농도(12.5±3.2、6.7±1.7)、심기세포조망솔[(27.9±5.3)％、(18.0±3.9)％]、GRP78 mRNA표체(0.95±0.07、0.62±0.06)화GRP78단백(769±132、542±98)표체균명현증가(P＜0.01)；E조여I/R조비교,cTnI농도、심기세포조망솔、GRP78 mRNA화GRP78단백표체균강저(P＜0.01).결론 재관주초기단잠산성복관액가조절GRP78적표체,조공ERS반응정도,감경내질망조망신호개도적세포조망발생,종이산생심기보호작용.
Objective To determine the effect of acidic reperfusion fluid to myocardial endoplasmic reticulum stress (ERS) glucose-regulated protein 78 (GRP78).Methods 24 SD rats were randomly divided into 3 groups (n =8).Control group (C),Isolated heart were only reperfused 180 min with pH 7.4 HEPES-KH.Ischemia/Reperfusion (I/R) group,isolated heart were reperfused 20 min and then ischemia for 60 min followed by 100 min reperfusion with pH 7.4 HEPES-KH.Experiment group (E),isolated heart were reperfused 20 min with pH 7.4 HEPES-KH and then ischemia for 60 min,and followed pH6.8,pH 7.1 and pH 7.4 HEPES-KH solution were reperfused 5-minute,5-minute,and 90-minute,respectively.Cardiac troponin Ⅰ (cTnI) concentration,apoptosis of myocardial cell,expressions of GRP78 mRNA and GRP-78 protein were detected.Results C group (1.3 ± 0.4,3.7 ± 1.1,0.43 ± O.04,384 ±75) Compared with 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 GRP78 mRNA (0.95 ±0.07,0.62 ±0.06) and expressions of GRP78 protein (769 ± 132,542 ± 98) increased significantly (P ＜ 0.01).Compared with I/R group,the cTnI concentration,apoptosis rote and expressions of GRP78 in E group were significantly lower (P ＜0.01).Conclusion Acidic reperfusion may protect the heart against L/R injury and alleviate ERS-mediated apoptosis after I/R by regulating expressions of GRP78.
