Chapat S, Frey V, Claperon N, Bouchaud C, Puisieux F, Couvreur P, Rossignol P, Delattre J
Laboratoire de Biochimie Métabolique et Clinique Université Paris.
Brain Res Bull. 1991 Mar;26(3):339-42. doi: 10.1016/0361-9230(91)90004-4.
This study was performed to elucidate the mechanism by which adenosine triphosphate (ATP) encapsulated into liposomes was able to protect against experimental brain ischemia in the rat. After intracarotidal administration of liposomally entrapped ATP, the ATP blood level increased dramatically whereas no change was observed after administration of free ATP. This suggested that liposomes may protect ATP from its degradation by endothelial ectonucleotidases. On the other hand, it was observed that after administration of liposomally entrapped carboxyfluorescein (CF) to ischemic rats, the distribution of the brain fluorescence under the form of numerous punctiform structures was completely different from the diffuse fluorescence obtained with free CF injections. These data suggest that under certain hypoxic conditions the blood-brain barrier is open allowing the liposomes to reach the cerebral parenchyma. The mechanism of brain uptake is, however, still unclear: endothelial tight junctions opening or endothelial transcytosis.
本研究旨在阐明包裹于脂质体中的三磷酸腺苷（ATP）能够保护大鼠免受实验性脑缺血损伤的机制。经颈动脉给予包裹有ATP的脂质体后，ATP的血药浓度显著升高，而给予游离ATP后则未观察到变化。这表明脂质体可能保护ATP不被内皮外切核苷酸酶降解。另一方面，观察到向缺血大鼠给予包裹有羧基荧光素（CF）的脂质体后，脑内荧光以众多点状结构的形式分布，这与游离CF注射后获得的弥漫性荧光完全不同。这些数据表明，在某些缺氧条件下，血脑屏障开放，使脂质体能够到达脑实质。然而，脑摄取的机制仍不清楚：是内皮紧密连接开放还是内皮转胞吞作用。
