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目的：通过制备出生后脑性瘫痪鼠模型并对鼠脑损伤进行评估，观察与人类孕期损伤导致婴儿脑组织前少突胶质细胞之间的关联。方法：新生乳鼠在出生后第3、4、5、6、7 天，每天腹腔注射脂多糖（LPS）（n=12，30,30,60,60,120μg/kg）或生理盐水（n=11）。新生乳鼠从生后第1 天至第21 天每天接受机能和认知发育测试。出生后第22 天对乳鼠脑组织进行免疫组织化学检测，通过对前少突胶质细胞标志物（CNP）及髓鞘标志物（MBP）的检测评估鼠脑白质损伤。神经发育测试数据采用重复测量方差分析方法，免疫组织化学实验数据采用方差分析方法。结果：对新生乳鼠进行神经生长发育测试后发现，LPS 处理组乳鼠在平面翻正测试、悬崖回避测试、前肢抓握测试及睁眼时间测试（P<0.05），活动力测试（P<0.01），其他几项比较无差异（P>0.05），悬吊实验（P>0.05），旷野实验（P<0.05）。前少突胶质细胞标志物CNP 在LPS 处理乳鼠组中是增多的（P<0.01），髓鞘碱性蛋白（MBP）在LPS 处理乳鼠组中是减少的（P<0.01）。结论：对新生乳鼠腹腔注射脂多糖可以引起鼠脑白质损伤，但是并不能出现与缺血缺氧模型一致的脑性瘫痪表型。

英文摘要:

Objective: Through the preparation of cerebral palsy rat model to evaluate damage of mouse brains, Observe postnatal CP model to evaluate injury that would correlate with presence of Pre-OL in human pregnancy. Methods: On postnatal (P) days2, 3, 4, 5 and 6, pups were treated with (lipopolysaccharide [LPS]) (n=12; 30, 30, 60, 60, 120 ug/kg) orsaline (n=11). Neonates were tested for motor and cognitive development. White matter damage was assessed with immunohistochemical Pre-OL markers (CNP, MBP). Statistical analysis included repeated measurements analysis of variance (ANOVA) was used where appropriate. Results: LPS-treated animals performed surface righting, cliff aversion, forelimb grasp and eye opening (P <0.05) and activity (P<0.01) and open field experiment (P<0.05). No differences were observed for other neonatal tests. Pre-OL markers were altered in LPS-treated animals at both P22 (CNP increased in LPS and MBP decreased in LPS, P<0.01). Conclusion: Neonatal exposure to LPS induce white matter damage in the brain, but these are similar to findings from a postnatal hypoxic model suggesting that in the rodent, targeting the Pre-OL does not result in a CP phenotype.

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