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目的:探讨不同放射性比活度32P对32P-磷酸铬-聚L-乳酸[32P-chromic phosphate-poly(L-lactide),32P-CP-PLLA]缓释粒子体内外溶蚀降解、放射性释出特性的影响。方法:将放射性比活度呈倍比增加的32P-CP-PLLA缓释粒子(记为S1-5)分别置于胎牛血清、生理盐水和右旋糖酐中(分别记为X、Y、Z组),另取S1-5型32P-CP-PLLA粒子分别植入肝癌HepG2实体瘤内,分别测定不同时间点粒子溶蚀降解失重率、放射性释出率及电镜下超微结构变化。结果:在胎牛血清(无菌环境下)、生理盐水及右旋糖酐中,相同时间点S1-5粒子放射性释出率增加,以32 d及其以后尤为显著,且相同时间点粒子放射性释出率增加呈一定的倍数关系;粒子肝癌内植入后,粒子降解失重率和放射性释出率随粒子放射性活度增加呈一致性增加,随时间变化的趋势同体外实验;胎牛血清(一般环境)中,粒子放射性释出较体内外其它组均快,差异以64 d显著,电镜下可见粒子内菌体存在。结论:32P作为一种纯β射线发射体,可能是32P-CP-PLLA粒子体内外降解和放射性释出的主要调节因素,而细菌或相关产物可能也是影响其降解的因素之一。
OBJECTIVE: To investigate the dissolution and degradation of 32P-chromic phosphate-poly (L-lactide), 32P-CP-PLLA sustained-release particles in vitro and in vivo with different radioactivity specific activity 32P Impact. Methods: The 32P-CP-PLLA sustained-release particles (denoted as S1-5) in multiples of radioactive specific activity were placed in fetal bovine serum, normal saline and dextran respectively (denoted as X, Y and Z groups) S1P-type 32P-CP-PLLA particles were implanted into HepG2 hepatocellular carcinoma respectively. The dissolution, degradation rate and radioactive release of the particles at different time points were measured respectively. The changes of ultrastructure were observed under electron microscope. Results: The radioactive release rate of S1-5 particles in fetal bovine serum (sterile environment), normal saline and dextran increased at the same time point, especially at 32 days and later, and at the same time point the radioactivity release rate Increase in a certain fold relationship; particle implantation in liver cancer, the rate of particle degradation and radioactive decay rate of radioactive particles with increasing activity was consistent increase with time trends in vitro experiments; fetal bovine serum (general environment) , The release of radioactive particles was faster than other groups in vitro and in vivo, the difference was significant at 64 d, the presence of intracellular particles was observed under electron microscope. CONCLUSIONS: 32P, as a pure beta-ray emitter, may be the main regulator of 32P-CP-PLLA particles in vitro and in vivo degradation and radioactive release, and bacteria or related products may also be one of the factors that affect their degradation.