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离体大鼠肝细胞与10~(-3)或10~(-4)mol/L的~3H-ATP共同孵化20分钟,细胞结合ATP量分别为0.53±0.06和0.21±0.03n mol/mg·Pr。应用脂质体作为药物载体包裹ATP(10~(-4)mol/L),使肝细胞结合ATP增加102.4％(P<0.01)。缺氧并不使细胞结合ATP增加。高浓度ATP(10~(-3)mol/L)降低正常或缺氧细胞存活率和增加细胞内蛋白漏出。10~(-4)mol/L的ATP对细胞存活率和蛋白漏出无明显影响,脂质体包裹的ATP抑制缺氧肝细胞的蛋白漏出。
Incubation of isolated rat hepatocytes with ~ 3H-ATP at 10 -3 or 10 -4 mol / L for 20 minutes incubated with 0.53 ± 0.06 and 0.21 ± 0.03n mol / mg ATP, respectively Pr. Application of liposomes as drug carrier to encapsulate ATP (10 ~ (-4) mol / L) increased the binding of hepatocytes to ATP by 102.4% (P <0.01). Hypoxia does not increase cellular binding of ATP. High concentrations of ATP (10 ~ (-3) mol / L) decreased normal or hypoxic cell viability and increased intracellular protein leakage. ATP at the concentration of 10 -4 mol / L had no significant effect on cell viability and protein leakage. Liposome-encapsulated ATP inhibited the protein leakage of hypoxic hepatocytes.