新生大鼠后天感染后脑白质中TRPM7和ANXA1的表达变化及意义

Change and significance of TRPM7 and ANXA1 expressions in celebral white matter of neonatal rats after acquired infection

目的观察新生大鼠生后感染后脑白质中TRPM7和ANXA1的表达变化,探讨新生大鼠感染后脑白质损伤的病理机制。方法将64只2 d龄SD大鼠随机分为对照组、实验组。实验组生后第2天开始腹腔注射脂多糖0.6 mg/kg(0.01ml/g),连用5 d,建立新生大鼠脑白质损伤模型;对照组等量生理盐水替代。注射后按观察时间点不同分为12 h、1 d、3 d、7 d 4个亚组(n=8)。处死大鼠时取出脑白质,HE染色后观察脑白质区病理变化;并用免疫组化和半定量RT-PCR法检测各组脑白质中TRPM7、ANXA1蛋白和mRNA水平的表达变化。结果实验组大鼠生长发育迟缓,脑白质病变明显,TRPM7和ANXA1在造模后12 h开始表达,1 d达高峰,随后下降,各时间点均高于对照组(P<0.05)。结论新生大鼠生后感染可引起脑白质损伤,TRPM7、ANXA1的高表达表明其可能参与了感染致脑白质损伤的病理过程。

Objective To observe the changes of TRPM7 and ANXA1 expressions in celebral white matter of neonatal rats after acquired infection,explore the pathological mechanism of cerebral white matter damage（ WMD） of neonatal rats after acquired infection.Methods Sixty- four two- day- old Sprague- Dawley（ SD） rats were randomly divided into control group and experimental group. The rats in experimental group were intraperitioneally injected with 0. 6 mg / kg（0. 01 ml / g） of lipopolysaccharide（ LPS） for five days from the second day after birth,then WMD model of neonatal rats was established; the rats in control group were treated by the same dose of normal saline. The rats in each group were divided into four subgroups according to observation time points： 12 hours,1 day,3 days,and 7 days,8 rats in each subgroup. Cerebral white matter specimens were obtained after killing the rats,pathological changes of cerebral white matter were observed after HE staining; immunohistochemical method and semiquantitative RT- PCR were used to detect the changes of TRPM7,ANXA1 proteins and mRNA in cerebral white matter of rats in different groups. Results Growth and development of rats in experimental group was slow,cerebral white matter lesions were obvious; the expression levels of TRPM7 and ANXA1 in experimental group started at 12 hours after establishing WMD model,reached the peak at 1 day,and then gradually declined. The expression levels in experimental group were statistically significantly higher than those in control group at each observation time point（ P〈0. 05）. Conclusion Acquired infection can lead to cerebral white matter lesions of neonatal rats,the high expressions of TRPM7 and ANXA1 indicate that they may be involved in the pathogenesis of WMD.