正常衰老过程中小鼠脑磷脂的动态转换及对缺血的反应。

G Y Sun, T N Lin
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引用次数: 0

摘要

采用体内标记方法研究了小鼠脑磷脂的动态转换,并评价了这些磷脂对斩首缺血性损伤的反应。在脑内注射[32P]-ATP后的4小时内,该标记有效地结合到所有磷脂中,并且在所检查的所有亚细胞膜组分中都是唯一的。就年龄而言,与10个月大的小鼠相比,从27个月大的小鼠组分离的突触体显示出更多的标签与多磷酸肌苷和磷脂酸结合,而与中性磷脂结合较低。随着年龄的增长,这些磷脂的标记增加似乎反映了磷酸化磷酸肌醇4-磷酸和二酰基甘油的底物基础水平的增加。底物水平的增加可能与磷肌苷循环中脂质代谢周转的减少有关。众所周知,斩首缺血性损伤会导致大脑中多磷酸肌苷的快速时间依赖性分解。然而,在10个月和27个月大的组中,缺血引起的多磷酸肌肽分解的比较并没有显示出它们消失率的明显年龄差异。
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Dynamic turnover of mouse brain phospholipids during normal aging and response to ischemia.

An in vivo labeling procedure was used to probe the dynamic turnover of mouse brain phospholipids and to evaluate the response of these phospholipids toward decapitation ischemic insult. Within 4 hr after intracerebral injection of [32P]-ATP, the label was effectively incorporated into all phospholipids and uniquely in all subcellular membrane fractions examined. With respect to age, synaptosomes isolated from the 27-month-old mice group showed a higher incorporation of label into polyphosphoinositides and phosphatidic acids and a lower incorporation into the neutral phospholipids than the 10-month-old group. The increase in labeling of these phospholipids with age seems to reflect the increase in basal level of substrates for phosphorylation of phosphoinositol 4-phosphate and diacylglycerols. The increase in substrate level is probably related to a decrease in metabolic turnover of the lipids underlying the phosphoinositide cycle. Decapitation ischemic insult is known to result in a rapid time-dependent breakdown of the polyphosphoinositides in brain. However, a comparison of the ischemia-induced breakdown of polyphosphoinositide between the 10 and 27 month-old groups did not reveal obvious age differences in the rate of their disappearance.

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