出生后炎症大鼠脑性瘫痪模型神经生长发育测试及脑组织 CNP、MBP 的表达

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。

The Research on Expression of CNP and MBP in Brain Damage of Postnatal Rats which were Treated by LPS and Nerve Growth Test

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)(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.