中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2010年
10期
1172-1174
,共3页
何祥虎%王焱林%颜学滔%王成夭%张宗泽%饶艳
何祥虎%王焱林%顏學滔%王成夭%張宗澤%饒豔
하상호%왕염림%안학도%왕성요%장종택%요염
血红素氧化酶(脱环)%细胞穿透肽类%心肌再灌注损伤
血紅素氧化酶(脫環)%細胞穿透肽類%心肌再灌註損傷
혈홍소양화매(탈배)%세포천투태류%심기재관주손상
Heme oxygenase(decyclizing)%Cell penetrating peptides%Myocardial reperfusion injury
目的 探讨细胞穿透肽PEP-1介导血红素加氧酶-1(HO-1)对大鼠离体心脏缺血再灌注损伤的影响.方法 雄性SD大鼠,体重220～280g,制备Langendorff离体心脏灌注模型,选取模型制备成功的离体心脏18个,随机分为3组(n=6):假手术组(S组)、缺血再灌注组(IR组)和PEP-1/HO-1处理+缺血再灌注组(HO-1组).IR组K-H液平衡灌注30 min后,采用停灌40 min再灌注50 min的方法制备缺血再灌注模型.HO-1组在停灌前用含50 μmol/L融合蛋白PEP-1/HO-1的K-H液平衡灌注15 min,S组采用K-H液持续灌注120 min.再灌注50 min时,收集冠脉流出液,测定肌酸激酶(CK)和乳酸脱氢酶(LDH)的活性;取心肌组织,采用Western blot法测定HO-1蛋白表达水平,采用硫代巴比妥酸比色法测定MDA含量,黄嘌呤氧化酶法测定SOD活性.结果 HO-1组心肌组织HO-1蛋白表达水平较IR组升高(P＜0.01).与S组比较,IR组和HO-1组冠脉流出液CK和LDH活性及心肌组织MDA含量升高,心肌组织SOD活性降低(P＜0.01);与IR组比较,HO-1组冠脉流出液CK和LDH活性及心肌组织MDA含量降低,心肌组织SOD活性升高(P＜0.01).结论细胞穿透肽PEP-1可将HO-1蛋白成功导入心肌组织,并减轻大鼠心肌缺血再灌注损伤.
目的 探討細胞穿透肽PEP-1介導血紅素加氧酶-1(HO-1)對大鼠離體心髒缺血再灌註損傷的影響.方法 雄性SD大鼠,體重220～280g,製備Langendorff離體心髒灌註模型,選取模型製備成功的離體心髒18箇,隨機分為3組(n=6):假手術組(S組)、缺血再灌註組(IR組)和PEP-1/HO-1處理+缺血再灌註組(HO-1組).IR組K-H液平衡灌註30 min後,採用停灌40 min再灌註50 min的方法製備缺血再灌註模型.HO-1組在停灌前用含50 μmol/L融閤蛋白PEP-1/HO-1的K-H液平衡灌註15 min,S組採用K-H液持續灌註120 min.再灌註50 min時,收集冠脈流齣液,測定肌痠激酶(CK)和乳痠脫氫酶(LDH)的活性;取心肌組織,採用Western blot法測定HO-1蛋白錶達水平,採用硫代巴比妥痠比色法測定MDA含量,黃嘌呤氧化酶法測定SOD活性.結果 HO-1組心肌組織HO-1蛋白錶達水平較IR組升高(P＜0.01).與S組比較,IR組和HO-1組冠脈流齣液CK和LDH活性及心肌組織MDA含量升高,心肌組織SOD活性降低(P＜0.01);與IR組比較,HO-1組冠脈流齣液CK和LDH活性及心肌組織MDA含量降低,心肌組織SOD活性升高(P＜0.01).結論細胞穿透肽PEP-1可將HO-1蛋白成功導入心肌組織,併減輕大鼠心肌缺血再灌註損傷.
목적 탐토세포천투태PEP-1개도혈홍소가양매-1(HO-1)대대서리체심장결혈재관주손상적영향.방법 웅성SD대서,체중220～280g,제비Langendorff리체심장관주모형,선취모형제비성공적리체심장18개,수궤분위3조(n=6):가수술조(S조)、결혈재관주조(IR조)화PEP-1/HO-1처리+결혈재관주조(HO-1조).IR조K-H액평형관주30 min후,채용정관40 min재관주50 min적방법제비결혈재관주모형.HO-1조재정관전용함50 μmol/L융합단백PEP-1/HO-1적K-H액평형관주15 min,S조채용K-H액지속관주120 min.재관주50 min시,수집관맥류출액,측정기산격매(CK)화유산탈경매(LDH)적활성;취심기조직,채용Western blot법측정HO-1단백표체수평,채용류대파비타산비색법측정MDA함량,황표령양화매법측정SOD활성.결과 HO-1조심기조직HO-1단백표체수평교IR조승고(P＜0.01).여S조비교,IR조화HO-1조관맥류출액CK화LDH활성급심기조직MDA함량승고,심기조직SOD활성강저(P＜0.01);여IR조비교,HO-1조관맥류출액CK화LDH활성급심기조직MDA함량강저,심기조직SOD활성승고(P＜0.01).결론세포천투태PEP-1가장HO-1단백성공도입심기조직,병감경대서심기결혈재관주손상.
Objective To investigate the protective effects of heme oxygenase-1 (HO-1) mediated by cell penetrating peptide PEP-1 on myocardium against ischemia/reperfusion (IR) injury in isolated rat hearts. Methods Healthy male SD rats weighing 220-280 g were anesthetized with intraperitoneal pentobarbital. Their hearts were excised and perfused in a Langendorff apparatus with K-H solution saturated with 95%O2-5% CO2 at 37 ℃. Eighteen isolated rat hearts were randomly divided into 3 groups ( n = 6 each): Ⅰ group sham operation (group S);Ⅱ group IR and Ⅲ group PEP-1/HO-1 + IR (group HO-1). The isolated rat hearts were perfused with an oxygena-ted (95% O2-5% CO2 ) K-H solution at 37 ℃ in a Langendorff apparatus and were subjected to 40 min of global ischemia followed by 50 min of reperfusion after 30 min of stabilization. In group Ⅲ (group HO- 1 ) the isolated hearts were perfused with 50 μmol/L PEP-1/HO-1 for 15 min before ischemia. After 50 min of reperfusion, HO-1expression, MDA content and SOD activity in myocardial tissues were determined. The activities of creatine kinase (CK) and lactic dehydrogenase (LDH) in coronary effluent fluid were measured. Results The HO- 1 expression was significanfly higher in HO-1 group than in group IR. IR induced significant increase in MDA content and decrease in SOD activity in myocardium and CK and LDH activities in coronary effluent in group Ⅱ compared with group S. PEP-1/HO-1 significantly attenuated IR-induced changes. Conciusion HO-1 mediated by PEP-1 has protective effects on myocardium ngainst IR injury in rats.
