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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 + 〕 i超载是胰腺腺泡细胞损伤和死亡的重要原因
Objective: To study the mechanism of hypoxia and reoxygenation induced pancreatic acinar cell injury. Methods: Hypoxia and reoxygenation were performed in isolated rat pancreatic acinar cells to observe the changes of pancreatic acinar cell survival and malondialdehyde (MDA) in different stages. At the same time, the changes of intracellular free calcium ion ([Ca2 +] i) labeled by fluorescent markers were detected by using the fluorescence spectrophotometer and image analysis system. Results: The survival rate of 4 h cells in control group was 78.0 9%, the survival rate of cells in hypoxia group at 4 h was 54.50% (P <0.05), the survival rate of cells in hypoxia 3 h and 1 h after reperfusion was 3 5.90% P <0.01). After 3 hours of hypoxia and 1 hour of reoxygenation, the intracellular [Ca2 +] i was significantly higher than that of the control group (P <0.05). The content of MDA in hypoxia and reoxygenation group was significantly higher than that in control group (P <0.01), and higher than that in hypoxia group (P <0.05). Conclusion: Hypoxia and reoxygenation can cause obvious damage of pancreatic acinar cells and cell death rate in rats. Acute injury caused more than simple hypoxia is more serious. Increased lipid peroxidation and intracellular [Ca2 +] i overload is an important cause of pancreatic acinar cell damage and death