摘要
目的:研究急性脊髓损伤和(或)内毒素攻击时小鼠肺组织中锌指蛋白A20的表达规律.方法:将昆明种小白鼠220只随机分为对照组(N组,n=10)、脊髓损伤组(A组,n=70)、内毒素组(B组,n=70)和脊髓损伤合并内毒素组(AB,n=70).以免疫组织化学(IHC),RT-PCR和HE染色分别检测肺组织中A20蛋白、mRNA和病理损害.结果:IHCN组A20蛋白微量表达(0.142±0.012);A组4～48 h较N组显著升高(P<0.05);B组0.5 h就出现高表达(0.202±0.020),0.5～24 h较N组显著升高(P<0.05),0.5～8 h较A组显著升高(P<0.05);AB组表达最强,0.5～48 h较N组显著升高(P<0.05),0.5～8 h较A组显著升高(P<0.05),8～48 h较B组显著升高(P<0.05).RT-PCR N组A20mRNA微量表达(0.883±0.033);A组4～24 h较N组显著升高(P<0.05);B组0.5～24 h较N组显著升高(P<0.05),0.5～4 h较A组显著升高(P<0.05);AB组表达最强,0.5～48 h较N组显著升高(P<0.05),0.5～24 h较A组显著升高(P<0.05),4～48 h较B组显著升高(P<0.05).HEAB组:0.5～4 h肺组织病理损害重,出现肺组织间质中性粒细胞浸润,上皮肿胀等,8 h以后病理损害较前有所减轻,但仍比N组重.结论:在脊髓损伤的早期肺组织即出现锌指蛋白A20表达增高,合并感染时尤其明显.说明在脊髓损伤(或合并感染)情况下,锌指蛋白A20表达增加可能对机体内源性调控过度的炎症具有重要意义.
Abstract
AIM: To study the expression of endogenous zinc finger protein A20 of mouse lung tissues in the process of spinal cord injury (SCI) and/or hpopolysaccharide (LPS) infection. METHODS : A total of 220 healthy mice ( from Kunming, Yun-nan Province ) were randomized into 4 groups: control group (group N), SCI group(group A), LPS group(group B) and SCI plus LPS group(group AB). The expressions of A20 protein and mRNA were measured by immunohistochemistry (IHC) and reverse transcription-polymerase chain reaction(RT-PCR) and the degree of pathological lesion was detected by HE staining. RESULTS: Both A20 protein and A20 mRNA expressed at low levels in group N and the highest expressions of A20 protein and A20 mRNA were observed in group AB, which reached peak respectively at 8 h and at 4 h, In group AB, severe pathologic damage of lung tissues was observed at 0.5 h. The severest damage was seen at 4 h and it began to alleviate after 8 h. CONCLUSION: In the early period of SCI, the expression of zinc finger protein A20 is high, especially in the case of LPS infection. The increased expression of A20 following SCI(or with LPS infection) may play an important role in regulating inflamma-tory response.
NETL
NSTL
维普
万方数据