中国医药
中國醫藥
중국의약
CHINA MEDICINE
2009年
7期
489-490
,共2页
心脏移植%肝细胞生长因子%心脏保存
心髒移植%肝細胞生長因子%心髒保存
심장이식%간세포생장인자%심장보존
Heart transplantation%Hepatocyte growth factor%Heart preservation
目的 研究肝细胞生长因子对大鼠供心长时间保存的保护作用并探讨其机制.方法 40只SD大鼠采用随机数字表法分为对照组20只和实验组20只,每组再分为2个亚组各10只.建立Langendorff-Neely灌注模型,分别用HTK液和加入重组人肝细胞生长因子100μg/L的HTK液作为停搏液和保存液.通过免疫组织化学方法 测定c-met受体;末端转移酶标记技术检测细胞凋亡指数;实时聚合酶链反应检测心肌bcl-2 mRNA的表达.结果 实验组c-met受体表达升高,凋亡指数降低,bcl-2 mRNA的表达升高,差异有统计学意义(均P<0.01).结论 肝细胞生长因子通过其特异性受体c-met的表达上调bcl-2 mRNA表达,减轻供心的细胞凋亡,产生有效的保护作用.
目的 研究肝細胞生長因子對大鼠供心長時間保存的保護作用併探討其機製.方法 40隻SD大鼠採用隨機數字錶法分為對照組20隻和實驗組20隻,每組再分為2箇亞組各10隻.建立Langendorff-Neely灌註模型,分彆用HTK液和加入重組人肝細胞生長因子100μg/L的HTK液作為停搏液和保存液.通過免疫組織化學方法 測定c-met受體;末耑轉移酶標記技術檢測細胞凋亡指數;實時聚閤酶鏈反應檢測心肌bcl-2 mRNA的錶達.結果 實驗組c-met受體錶達升高,凋亡指數降低,bcl-2 mRNA的錶達升高,差異有統計學意義(均P<0.01).結論 肝細胞生長因子通過其特異性受體c-met的錶達上調bcl-2 mRNA錶達,減輕供心的細胞凋亡,產生有效的保護作用.
목적 연구간세포생장인자대대서공심장시간보존적보호작용병탐토기궤제.방법 40지SD대서채용수궤수자표법분위대조조20지화실험조20지,매조재분위2개아조각10지.건립Langendorff-Neely관주모형,분별용HTK액화가입중조인간세포생장인자100μg/L적HTK액작위정박액화보존액.통과면역조직화학방법 측정c-met수체;말단전이매표기기술검측세포조망지수;실시취합매련반응검측심기bcl-2 mRNA적표체.결과 실험조c-met수체표체승고,조망지수강저,bcl-2 mRNA적표체승고,차이유통계학의의(균P<0.01).결론 간세포생장인자통과기특이성수체c-met적표체상조bcl-2 mRNA표체,감경공심적세포조망,산생유효적보호작용.
Objective To observe the effect of hepatocyte growth factor on isolated rat heart preservation. Methods Forty SD mrs were randomly divided into two groups : control group (n = 20) with isolated rat heart preserved in 4 ℃ HTK solution and experimental group(n =20) with isolated rat hearts preserved in 4 ℃ HTK + rh-HGF(100 μg/L) solution. Cell apoptosis was detected by TUNEL staining and the expression of bcl-2mRNA was examined by RT-PCR. Results Experimental group showed a lower rate of apoptosis eardiomyocytes (P < 0.01) after reperfusion. Immunohistochemieal analysis revealed that c-met receptor expression was stronger in the HGF-treated myocardium than that in the non-HGF-treated myocardium after storage and was associated with a stronger ex-pression of bcl-2 mRNA. Conclusion The administration of rh-HGF before storage improved cardiac function after prolonged myocardial preservation by preventing apoptosis and enhancing expression of bcl-2 mRNA.