缺氧再复氧对大鼠离体胰腺细胞损伤的机制

The mechanism of isolated pancreatic acinar cell injury during hypoxia-reoxygenation in rats

目的 :对缺氧再复氧引起胰腺腺泡细胞损伤的机制进行研究。方法 :通过对离体胰腺腺泡细胞给予缺氧再复氧处理 ,观察不同阶段胰腺腺泡细胞的存活率 ,脂质过氧化产物丙二醛 ( MDA)的变化。同时应用显微荧光分光光度计和图象分析系统检测被荧光标记物标记的细胞内游离钙离子 (〔Ca2 +〕i)浓度的变化。结果 :对照组 4 h细胞存活率为 78.0 9% ,缺氧组 4 h细胞存活率 54.50 % ( P<0 .0 5) ,缺氧3 h再复氧 1 h细胞存活率为 3 5.90 % ( P<0 .0 1 ) ,缺氧 3 h再复氧 1 h,细胞内〔Ca2 + 〕 i较对照组明显升高 ( P<0 .0 5)。缺氧再复氧组 MDA含量较对照组明显增多 ( P<0 .0 1 ) ,且高于缺氧组 ( P<0 .0 5)。结论 :缺氧再复氧可引起大鼠胰腺腺泡细胞明显损伤 ,细胞死亡率上升。比单纯缺氧造成的急性损伤更为严重。脂质过氧化反应的增加和细胞内〔Ca2 + 〕

Objective:The present study was aimed to investigate the mechanism of isolated pancreatic acinar cell injury during hypoxiareoxygenation in rats.Methods:The intracellular free calcium(〔Ca 2+ 〕i)concentration in pancreatic acinar cell were measured by OPTON 30 UMP fluorescence microspectrophoto meter.〔Ca 2+ 〕i of marked fluorescent indicator Fura 2AM were analyzed by digital image processing system.Lipid peroxidized product Malondialdeyhde (MDA) and pancreatic acinar cell mortality were examined.Results:With extended hypoxia time,the pancreatic acinar intracellular 〔Ca 2+ 〕i rose gradually.At reoxygenation one hour after hypoxia three hours,intracellular 〔Ca 2+ 〕i increased significantly( P <0 01).MDA content was similar to 〔Ca 2+ 〕i change.Survival rates of normal,hypoxia four hours and reoxygenation one hour after hypoxia three hours groups approximate to 78 09%,54 50% and 35 90% respectively.Conclusion:Hypoxia reoxygenation might have caused obviously injury of isolated pancreatic acinar cell.Both lipid peroxidized reaction and intracellular calcium overload were main mechanism of hypoxiareoxygenation injury.