摘要
目的观察苏木乙酸乙酯提取物对同种异位心脏移植大鼠移植心肌GrB mRNA表达的影响,探讨苏木免疫活性部位抗排斥反应作用机理。方法以Wistar大鼠为供体,以SD大鼠为受体,建立大鼠腹腔异位心脏移植模型,将手术成功鼠随机分为模型组、苏木组、环孢素A(CsA)组,采用RT-PCR法检测GrB mRNA表达。常规方法观察心肌病理形态学。结果(1)病理组织学分级:与模型组(积分31)比较,CsA组(积分14)和苏木组(积分23)均能减轻移植心肌病理损伤(P<0.05,P<0.01)。(2)移植心肌组织GrB mRNA的表达:与模型组(1.3000±0.1207)比较,CsA组(0.6700±0.0997)和苏木组(0.7070±0.1215)能明显下调GrB mRNA表达(P<0.01),CsA组与苏木组比较,差异无统计学意义(P>0.05)。结论苏木乙酸乙酯提取物能够减轻移植心脏心肌的病理损伤,能够下调大鼠移植心脏心肌GrB的基因表达,这可能是抗急性排斥反应因素之一。
Objective To explore the action mechanism of the immune active components of sappon wood (SWE) for antagonizing reject reaction by observing the influence of its ethyl acetate extract on mRNA expression of myocardial GrB in rat model of allogenic ectopic cardiac transplantation. Methods Animal model of abdominal cardiac ectopic transplantation was established taking Wistar rat as the donor and SD rat as the receptor. The successfully modeled rats were randomly divided into the model group, the SWE group and the CsA group. GrB mRNA expression was detected by RT-PCR method and myocardial pathomorphologic picture was observed in routine. Results The pathologic changes in the SWE group (23 scores) and the CsA group (14 scores) were milder than in the model group (31 scores) , the former two could markedly alleviate the myocardial pathologic injury (P 〈0. 05, P 〈0. 01 ). The GrB mRNA expression in the model group was 1. 3000 ± 0. 1207, the SWE group 0. 7070 ± 0. 1215, and the CsA group 0. 6700 ±0. 0997, respectively; compared with the model group, the latter two could obviously down-regulate the expression of GrB mRNA (P 〈0.01 ) and no significant difference was found between the latter two groups ( P 〉 0. 05 ). Conclusion SWE could alleviate the pathologic change, down-regulate the mRNA expression of myocardial GrB in allogenic ectopic transplanted myocardium of rats, it is possibly one of the factors for its antagonizing effect against reject reaction.
出处
《中国中西医结合杂志》
CAS
CSCD
北大核心
2008年第6期537-540,共4页
Chinese Journal of Integrated Traditional and Western Medicine
基金
黑龙江省科学计划攻关项目(N0.20010101002-00)