中国实用医刊
中國實用醫刊
중국실용의간
CENTRAL PLAINS MEDICAL JOURNAL
2013年
18期
33-34
,共2页
张新%高颖欣%罗鸿%张伟华%黄秋霞%乔晨晖
張新%高穎訢%囉鴻%張偉華%黃鞦霞%喬晨暉
장신%고영흔%라홍%장위화%황추하%교신휘
多粘菌素B%Bcl-2%大鼠%肺移植
多粘菌素B%Bcl-2%大鼠%肺移植
다점균소B%Bcl-2%대서%폐이식
Polymyxin B%Bcl-2%Rat%Lung transplantation
目的 研究多粘菌素B对大鼠移植肺中Bcl-2表达的影响,探讨缺血预适应对大鼠移植肺保护的机制.方法 在大鼠左肺移植模型基础上分别采用缺血预适应及多粘菌素B灌注肺动脉,观察对移植肺Bcl-2表达的影响.结果 缺血预适应组与对照组、多粘菌素B组左肺静脉血氧分压、细胞凋亡指数、Bcl-2表达比较差异有统计学意义(P<0.05),对照组与多粘菌素B组比较差异无统计学意义(P>0.05).结论 肺组织中缺血预适应保护机制可能为蛋白激酶C活化;多粘菌素B能使蛋白激酶C失活,导致Bcl-2表达下调,引起细胞凋亡.
目的 研究多粘菌素B對大鼠移植肺中Bcl-2錶達的影響,探討缺血預適應對大鼠移植肺保護的機製.方法 在大鼠左肺移植模型基礎上分彆採用缺血預適應及多粘菌素B灌註肺動脈,觀察對移植肺Bcl-2錶達的影響.結果 缺血預適應組與對照組、多粘菌素B組左肺靜脈血氧分壓、細胞凋亡指數、Bcl-2錶達比較差異有統計學意義(P<0.05),對照組與多粘菌素B組比較差異無統計學意義(P>0.05).結論 肺組織中缺血預適應保護機製可能為蛋白激酶C活化;多粘菌素B能使蛋白激酶C失活,導緻Bcl-2錶達下調,引起細胞凋亡.
목적 연구다점균소B대대서이식폐중Bcl-2표체적영향,탐토결혈예괄응대대서이식폐보호적궤제.방법 재대서좌폐이식모형기출상분별채용결혈예괄응급다점균소B관주폐동맥,관찰대이식폐Bcl-2표체적영향.결과 결혈예괄응조여대조조、다점균소B조좌폐정맥혈양분압、세포조망지수、Bcl-2표체비교차이유통계학의의(P<0.05),대조조여다점균소B조비교차이무통계학의의(P>0.05).결론 폐조직중결혈예괄응보호궤제가능위단백격매C활화;다점균소B능사단백격매C실활,도치Bcl-2표체하조,인기세포조망.
Objective To study the effect of ploymyxin B on Bcl-2 expression,and the protective mechanism of ischemic preconditioning on rat lung transplantation.Methods Based on the model of lung transplantation in rat,ischemic preconditioning and ploymyxin B was used,respectively,and the effects on expression of Bcl-2 in transplanted lung were observed.Results Compared with ploymyxin B group and control group,the blood oxygen of left pulmonary veins,apoptosis index and the expression of Bcl-2 of ischemic preconditioning group were significantly different (P < 0.05),there was no significant difference between ploymyxin B group and control group (P > 0.05).Conclusions Lung protective mechanism of ischemic preconditioning may be protein kinase C activation;Polymyxin B can make PKC deactivation,thereby down-regulation the expression of Bcl-2,and then arouse the apoptosis of the cells.