摘要
目的探讨宫内感染致早产鼠脑白质损害的机制。方法30只Wistar孕鼠分为实验组18只和对照组12只,在妊娠第15、16天,对实验组孕鼠连续2d腹腔内注射脂多糖(LPS)0.2mg/kg,对照组孕鼠注射等量蒸馏水;取实验组早产鼠45只、对照组足月鼠45只,采用放免法(RIA)测定两组鼠脑组织白细胞介素6(IL-6)含量;另取实验组早产鼠47只,对照组足月鼠41只,对脑组织进行HE染色;再取50只实验组早产鼠及50只对照组足月鼠进行脑组织含水量测定。结果实验组早产鼠脑组织IL-6含量明显高于对照组足月鼠(P<0.01),脑组织含水量较对照组足月鼠明显增高(P<0.01);早产鼠脑组织切片均见脑室周围白质水肿,神经毡疏松化,细胞成分明显减少,神经细胞间隙增宽,细胞肿胀、破裂;对照组足月鼠脑组织形态结构未见异常。结论细菌内毒素可导致早产鼠脑白质损害,且脑组织中IL-6及含水量均增高。
Objective To investigate the mechanism of cerebral white matter damage in premature rats induced by intrauterine infection. Methods 30 mature pregnant Wistar-Imamichi rats were divided into the experimental group (n= 18) and control group (n= 12). The rats of the experimental group were injected with lipopolysaccharide (LPS) 0.2 mg/kg in abdomen on 15th and 16th day after gestation. Those of the control group were injected with distilled water in equal volume. 45 premature rats born in the experimental group and 45 full-term rats born in the control group were tested with RIA for interleukin-6 (IL-6). The brain tissues of another 47 premature rats and 41 full-term rats were stained with HE method. Finally water content in brain tissue were tested in 50 premature rats and 50 full-term rats. Results IL-6 concentration of brain tissue of the premature rats in the experimental group was significantly higher than that in the control group ( P d0.01) ; and water content of the premature rats' brain was also higher than that of the full-term rats ( P 〈0.01). The edema of periventricular white matter, loose neuropil, decreased cell numbers, broaden intercellular space, and cell swelling and rupture were found in the brain tissue of the premature rats, no abnormal form and structure were found in the control group. Conclusion White matter damage of premature rats can be caused by endotoxin, and accompanied by IL-6 and water contents increasing.
出处
《中国康复理论与实践》
CSCD
2006年第10期829-830,F0003,共3页
Chinese Journal of Rehabilitation Theory and Practice
关键词
脂多糖
脑瘫
脑白质损害
lipopolysaccharide
cerebral palsy
white matter damage