摘要
目的观察缺血预处理对大鼠冷保存供肝细胞HMG-CoA还原酶（HMGCR）活力的影响，探讨缺血预处理减轻大鼠供肝冷保存损伤的机制。方法将25只大鼠随机分为对照组（C组）、冷保存组（I组）、缺血预处理组（IP组）、阿托伐他汀30μmol／L和100μmol／L处理组（A30组和A100组），每组5只。C组为正常大鼠肝脏，4℃ UW液灌注；I组为灌注后冷保存8h；IP组先给予缺血预处理，灌注后冷保存8h；A30组和A100组先给予缺血预处理，用终质量浓度为30μmol／L和100μmol／L的阿托伐他汀UW液灌注后再置入含30μmol／L和100μmol／L的阿托伐他汀UW液中4℃冷保存8h。分别测定5组大鼠肝脏的HMGCR活力。结果供肝经过8h冷保存后（I）HMGCR活性为（1872±157）nmol／（min·mg），与对照组（C）（3298±224）nmol／（min·mg）比较明显下降（P〈0．05），给予缺血预处理后再给予冷保存（IP），则HMGCR活性为（3746±231）nmol／（min·mg），明显升高（P〈0．05）；给予缺血预处理同时给予HMGCR抑制剂阿托伐他汀则HMGCR活性则受到明显抑制，并随着阿托伐他汀浓度的增加而抑制效应更为明显，A30组、A100组HMGCR酶活力分别为（2010±193）nmol／（min·mg）、（1469±132）nmol／（min·mg），同IP组比较明显下降（P〈0．05）。结论缺血预处理可以明显提高HMGCR活力，而阿托伐他汀则可消除缺血预处理升高HMGCR活性的作用；缺血预处理升高HMGCR活力的机制是增加HMGCR蛋白的表达。
Objective To investigate the effects of ischemic preconditioning on the activity of 3- hydroxy-3-methylglutary coenzyme A reduetase （HMGCR） of hepatoeytes following eryopreservation in rats. Methods Twenty-five rats were randomly divided into five groups ： control group （C） , eryopreservation group （ I）, isehemie preconditioning group （ IP）, atorvastatin （ 30μmol/L） treatment group （A30） and atorvastatin （100 p, mol/L） treatment group （A100）. In control group, normal donor livers were flushed with 4 ℃ UW solution. In group I, donor livers were cryopreserved for 8 h after UWs flushing. In group IP, donor livers were subjected to ischemic preconditioning, and then flushed and eryopreserved in UWs. In group A30, donor livers were treated as in group I except that 30 μmol/L atorvastatin was added to the UWs. In group A100, donor livers were treated as in group I with the exception that 100 p,mol/L atorvastatin was added to the UWs. The activity of HMGCR was assessed. Results HMGCR activity in the donor liver was significantly decreased after cryopreservation for 8 h [ （ 1872 ± 157） nmo]/（min.mg） ], and significantly increased after ischemic preconditioning [ （ 3746 ± 231 ） nmol/（ min· mg） ]. The enhanced HMGCR activity induced by isehemic preconditioning was inhibited by atorvastatin in a concentration-dependent manner. In groups A30 and A100, HMGCR activity was [ （2010 ± 193） nmol/（min.mg） ] and [ （ 1469 ± 132） nmol/（ min·mg）] respectively. Conchlsion Ischemic preconditioning significantly enhances HMGCR activity by up-regulating its protein expression and this effect can be abrogated by atorvastatin.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2011年第8期1315-1317,共3页
Chinese Journal of Experimental Surgery
基金
基金项目：国家自然科学基金资助项目（30972951）
国家科技支撑计划资助项目（2008BAl60802）
广东省自然科学基金资助项目（06104600）
关键词
肝细胞
缺血预处理
冷保存
HMG—CoA还原酶
Hepatocytes
Ischemie preconditioning
Cold preservation
3-hydroxy-3-methylglutary eoenzyme A reduetase
