肝脏低温保存-再灌注后的变化及机制

目的　研究肝脏低温保存 再灌注期间 ,肝细胞糖原含量与肝细胞凋亡之间的关系及其相关机制。方法　制备四组肝糖原含量显著不同的兔肝脏模型 ,肝糖原含量 (mg/ g)分别为 :A组 :15 .42± 2 .6 0 ;B组 :5 1.83± 6 .6 1;C组 :6 3 .2 2± 5 .84;D组 :78.5 8± 8.46。检测各组肝脏低温保存 再灌注过程中肝细胞凋亡及组织内氧自由基相关指标 (SOD、GSH、MDA)的变化情况。结果　各组肝脏低温保存 9h后 ,再灌注 6 0min时 ,组织内可见明显的肝实质细胞凋亡现象 ,其凋亡细胞数量依次为A组 >B组 >C组 >D组 ,四组间差异均有显著性 ;且此时各组肝脏组织中SOD、GSH或MDA水平差异也均有显著性。结论　肝脏低温保存 再灌注过程中 ,肝细胞内糖原能显著拮抗肝实质细胞凋亡的发生 ;其内在机制可能在于肝细胞糖原通过抑制氧自由基的产生而达到拮抗肝实质细胞凋亡的发生。

Ralationship between hepatocellular apoptosis and glycogen contents during cold preservation-reperfusion of liver and its mechanism

Objective To study relationship between hepatocellular apoptosis and glycogen contents during cold preservation-reperfusion of liver and its mechanism. Methods Rat liver models with different contents of glycogen were established and the rats were divided into 4 groups (A, B, C and D). During cold reservation-reperfusion of liver, the changes in hepatocellular apoptosis and tissue SOD, GSH and MDA were observed in the groups. Results After cold preservation for 9 h in each group, 60?min reperfusion could result in obvious apoptosis in livers. There was difference in the numbers of apoptotic hepatocytes among all the groups. At the same time, there also were significant difference in the levels of SOD, GSH and MDA in liver tissue among the four groups.Conclusion Intracellular abundant glycogen may significantly depress hepatocellular apoptosis during hepatic cold preservation-reperfusion by decressing oxygen free radicals.