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(inositol1,4,5triphosphatereceptors,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.
出处
《北京医科大学学报》
CSCD
1999年第4期306-308,314,共4页
Journal of Peking University(Health Sciences)
关键词
败血病
肝细胞内核膜
受体
三磷酸肌醇
Septicemia Liver Cell nucleus Inositol 1,4,5 triphosphate Receptors