作　　者： ;

机构地区： 广东省深圳市福田区第二人民医院翰岭社区健康服务中心广东深圳518049

出　　处： 《心血管康复医学杂志》 2018年第3期247-250,共4页

摘　　要： 目的:分析钙敏感受体/胱硫醚-γ-裂解酶-硫化氢(CaR-CaM/CSE-H_2S)路径对缺血再灌注相关氧化应激的影响。方法:选择50只胱硫醚-γ-裂解酶(Cystathionine-gamma-lyase,CSE)基因敲除大鼠作为CSE基因敲除组,另选同期50只正常大鼠为正常对照组。仅CSE基因敲除组大鼠建立心肌缺血再灌注损伤模型。测量比较两组血浆总抗氧化能力、活性氧、超氧化物歧化酶(SOD)、丙二醛(MDA)水平、细胞凋亡指标(Bax,Bcl-2,Caspase-3mRNA,Caspase-8mRNA,Caspase-9mRNA)表达、钙敏感受体(CaR)表达水平、CSE活性和H_2S含量。结果:与正常对照组比较,CSE基因敲除组血浆总抗氧化能力[(11.78±1.14)U/ml比(10.20±1.25)U/ml]、SOD水平[(772.79±5.21)nmol/L比(558.94±5.36)nmol/L]、CaR表达水平[(2.85±1.01)%比(1.04±0.33)%]、CSE活性[(18.30±1.70)nmol·L^(^(-1))·min^(-1)·g蛋白比(11.50±1.50)nmol·L^(^(-1))·min^(-1)·g蛋白]以及H_2S含量[(48.55±1.35)μmol/g蛋白比(30.59±1.41)μmol/g蛋白]均显著降低,活性氧[(90.48±1.42)U/ml比(99.74±1.45)U/ml]、MDA水平[(4.33±1.15)U/ml比(4.98±1.12)U/ml]、细胞凋亡指标Bax[(0.25±0.05)比(0.47±0.23)]、Bcl-2[(0.18±0.02)比(0.35±0.05)]、Caspse-3 mRNA[(0.16±0.04)比(0.25±0.05)]、Caspse-8mRNA[(0.20±0.10)比(0.44±0.15)]和Caspse-9mRNA[(0.05±0.01)比(0.15±0.05)]表达均显著升高,P均<0.01。结论:缺血再灌注过程中冠脉血管内皮CaR表达下调,CSE活性降低,内源性H_2S生成减少,加重缺血再灌注引起的氧化应激损伤。 Objective：To analyze influence of calcium sensitive receptor/cystathionine-γ-lyase hydrogen sulfide（CaRCaM/CSE-H_2 S）pathway on ischemia reperfusion（I/R）related oxidative stress.Methods：A total of 50 CSE gene knockout rats were selected as CSE gene knockout group,another 50 normal rats were simultaneously enrolled as normal control group.Myocardial ischemia reperfusion injury（MIRI）model was established in only CSE gene knockout group.Plasma total antioxidant capacity,levels of reactive oxygen species（ROS）,superoxide dismutase（SOD）and malonyl diadehyde（MDA）,expressions of cell apoptosis indexes（Bax,Bcl-2,Caspase-3 mRNA,Caspase-8 mRNA,Caspase-9 mRNA）,calcium sensitive receptor（CaR）expression,CSE activity and H_2 S content were measured and compared between two groups.Results：Compared with normal control group,there were significant reductions in plasma total antioxidant capacity[（11.78±1.14）U/ml vs.（10.20±1.25）U/ml],SOD level[（772.79±5.21）nmol/L vs.（558.94±5.36）nmol/L],CaR expression[（2.85±1.01）% vs.（1.04±0.33）%],CSE activity[（18.30±1.70）nmol·L^-1·min^-1·g prot vs.（11.50±1.50）nmol·L^-1·min^-1·g prot]and H_2 S content[（48.55±1.35）μmol/g prot vs.（30.59±1.41）μmol/g prot],and significant rise in levels of ROS[（90.48±1.42）U/ml vs.（99.74±1.45）U/ml]and MDA [（4.33±1.15）U/ml vs.（4.98±1.12）U/ml],expressions of Bax [（0.25±0.05）vs.（0.47±0.23）],Bcl-2 [（0.18±0.02）vs.（0.35±0.05）],Caspse-3 mRNA[（0.16±0.04）vs.（0.25±0.05）],Caspse-8 mRNA [（0.20±0.10）vs.（0.44±0.15）]and Caspse-9 mRNA[（0.05±0.01）vs.（0.15±0.05）]in CSE gene knockout group,P〈0.01 all.Conclusion：During I/R,coronary endocardial CaR expression down regulates,CSE activity reduces and endogenous H_2 S generation decreases,which aggravate oxidative stress injury caused by I/R.

关 键 词： 再灌注损伤 氧化性应激 内皮 血管

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