败血症大鼠肝细胞内核膜三磷酸肌醇受体的改变  

Changes of inositol 1,4,5 triphosphate receptors in inner nuclear membrane of rat liver during sepsis

作　　者：郝胜利[1,2] 杨军[1,2] 张孙曦 庞永政[1,2] 苏静怡 唐朝枢[1,2] 

机构地区：[1]北京医科大学生物物理系 [2]第一医院心血管研究所

出　　处：《北京医科大学学报》1999年第4期306-308,314,共4页Journal of Peking University(Health Sciences)

摘　　要：目的：观察早期、晚期败血症大鼠肝细胞内核膜上１，４，５三磷酸肌醇受体（ｉｎｏｓｉｔｏｌ１，４，５ｔｒｉｐｈｏｓｐｈａｔｅｒｅｃｅｐｔｏｒｓ，ＩＰ３Ｒ）的变化。方法：通过结扎并穿刺盲肠制作大鼠败血症模型，差速离心分离内核膜，［３Ｈ］ＩＰ３放射配体分析肝内核膜ＩＰ３Ｒ与其配体的最大结合容量（Ｂｍａｘ）及亲和力（Ｋｄ）。４５Ｃａ２＋转运测定内核膜ＩＰ３Ｒ释放Ｃａ２＋功能。结果：早期和晚期败血症Ｂｍａｘ分别增加１４％（Ｐ＜０．０５）和９１％（Ｐ＜０．０１）。但Ｋｄ值无明显变化（Ｐ＞０．０５）。ＩＰ３引起４５Ｃａ２＋转运在败血症时也相应增加。结论：在败血症时肝细胞核被膜ＩＰ３Ｒ发生上调，其释放Ｃａ２＋的能力增强，但结构可能未发生变化。Objective: To investigate the changes of inositol triphosphate receptors in the inner nuclear membrane of rat liver during sepsis. Methods: Septic rat model was prepared by cecal ligation and puncture (LCP). The binding site density (B max ) and affinity (K d) of IP 3 to the inner nuclear membrane were measured by IP 3 binding assay. The function of IP 3 receptors to release Ca 2+ was assessed by 45 Ca 2+ movement to the inner nuclear membrane vesicle upon the action of IP 3. Results: B max was increased by 14% ( P <0.05) during early sepsis and by 91% ( P <0.01) during late sepsis while no alterations of the affinity of IP 3R to its ligand was shown during sepsis. 45 Ca 2+ movement to the inner nuclear membrane vesicle was also increased accordingly during sepsis. Conclusion: Binding site density and the function of IP 3R in the inner nuclear membrane were progressively increased during sepsis, while there might be no change in the structure.

关 键 词：败血病 肝细胞内核膜 受体 三磷酸肌醇 

分 类 号：R631.3[医药卫生—外科学]