Effects of ischemic preconditioning on cholesterol content and activity of Na+ -K+ -ATPase of hepatocytes following cold preservation in rats
10.3760/cma.j.issn.0254 1785.2012.03.007
- VernacularTitle:缺血预处理减轻大鼠供肝冷保存损伤的作用及其机制
- Author:
Weiqiang JU
;
Zhipeng WU
;
Xiaoshun HE
;
Zhiyong GUO
;
Linwei WU
;
Dongping WANG
;
Xiaofeng ZHU
;
Jiefu HUANG
- Publication Type:Journal Article
- Keywords:
Rats;
Liver;
Organ preservation;
Injuries;
Ischemic preconditioning
- From:
Chinese Journal of Organ Transplantation
2012;33(3):156-159
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of ischemic preconditioning on the cholesterol content and the activity of Na+-K+-ATPase of hepatocytes following cold preservation in rats.Methods Twenty-five rats were randomly divided into five groups,including control group (C),cold preservation group (Ⅰ),ischemic preconditioning group (ⅠP),atorvastatin (30 μmol/L) treatment group (A30),and atorvastatin (100 μmol/L) treatment group (A100).The cholesterol content and the activity of Na+ -K+ -ATPase were assessed.Results The cholesterol contents on the rat liver tissue cell membrane in the C group,Ⅰ group,ⅠP group,A30 group and A100 group were (310.4 ± 27.5),(187.7±13.1),(394.3±25.9),(201.8±14.6) and (122.6±7.7) nmol/mg protein,and activity of the Na+ -K+ -ATP enzyme was (46.55 ± 3.20),(27.4 ± 2.81),(52.71 ± 3.02),(30.67 ±2.78) and (19.64 ± 2.11) μmol Pi/hr mg protein,respectively (P＜0.05).There was no significant difference in the plasma membrane phospholipid content among the five groups (P＞0.05).Conclusion Reduction of cholesterol content and Na+ K+ -ATPase activity on the liver cytoplasmic membrane is one of the factors causing donor liver cold preservation injury,but ischemic preconditioning can significantly improve cell membrane Na+ -K+ -ATPase activity and increase cytoplasmic membrane cholesterol content. Use of atorvastatin statins can reduce cytoplasmic membrane cholesterol synthesis,and significantly decrease Na+ -K+ -ATPase activity,thereby alleviating the donor liver cold preservation injury.
