CAJ | 학술논문

目的：探讨重组人促红细胞生成素（ rhEPO）对压力超负荷大鼠心室肥厚的干预作用及机制。方法通过腹主动脉缩窄法建立大鼠压力超负荷诱导的心室肥厚模型后，将大鼠随机分为假手术组（ Sham组），模型组（ AAC组），rhEPO干预组（ rhEPO组），4周后处死大鼠，计算左室质量指数，心肌常规HE染色观察心室肌病理变化，分别用黄嘌啉氧化酶法、比色法检测心肌中丙二醛（ MDA）、超氧化物歧化酶（ SOD）含量。用双夹心ELISA法测定心室组织的肿瘤坏死因子－α（TNF－α）含量，比较各组差异。结果4周后AAC组大鼠心肌显示明显的心肌肥厚，心室质量指数、MDA以及TNF－α的含量与Sham组大鼠比较均明显增高，而SOD的含量显著降低（ P＜0．01）。rhEPO干预后大鼠未显示明显的心肌肥厚，与AAC组大鼠相比，心室质量指数、MDA以及TNF－a的含量明显降低，SOD的含量则增高（P＜0．01）。结论 rhEPO可以抑制压力超负荷诱导的心室肥厚的形成，其部分机制可能与其抑制心肌中的过氧化反应及抗炎效应有关。
목적：탐토중조인촉홍세포생성소（ rhEPO）대압력초부하대서심실비후적간예작용급궤제。방법통과복주동맥축착법건립대서압력초부하유도적심실비후모형후，장대서수궤분위가수술조（ Sham조），모형조（ AAC조），rhEPO간예조（ rhEPO조），4주후처사대서，계산좌실질량지수，심기상규HE염색관찰심실기병리변화，분별용황표람양화매법、비색법검측심기중병이철（ MDA）、초양화물기화매（ SOD）함량。용쌍협심ELISA법측정심실조직적종류배사인자－α（TNF－α）함량，비교각조차이。결과4주후AAC조대서심기현시명현적심기비후，심실질량지수、MDA이급TNF－α적함량여Sham조대서비교균명현증고，이SOD적함량현저강저（ P＜0．01）。rhEPO간예후대서미현시명현적심기비후，여AAC조대서상비，심실질량지수、MDA이급TNF－a적함량명현강저，SOD적함량칙증고（P＜0．01）。결론 rhEPO가이억제압력초부하유도적심실비후적형성，기부분궤제가능여기억제심기중적과양화반응급항염효응유관。
Objective To investigate the effect of rhEPO on left ventricular hypertrophy induced by pressure-overload in rats.Methods The rat model were established by coarctation of abdominal aorta ( AAC) in Wister rats.Rats were randomly allocated to three groups:Sham group, AAC group, rhEPO group.Rats in rhEPO group were injected rhEPO (1000 U/kg) subcutaneously for three times a week after operation.Rats in Sham group were given the same volume of physiological saline.All rats were killed after 4 weeks.Left ventricular mass index ( LVMI) was calculated.Myocardial histological changes were observed with routine HE stain, and the level of SOD, MDA, TNF-αin myocardium were detected respec-tively.Results Compared with the sham group, there were significant cardiac hypertrophy, higher LVWI and level of MDA and TNF-α(P<0.01), while lower SOD level (P<0.01) in myocardium in rats of AAC group.However, compared with the AAC group, cardiac hypertrophy was significantly relieved in rhEPO group, as well as LVMI and the levels of MDA, TNF-αdecreased, SOD level improved in myocardium (P<0.01).Conclusion RhEPO could attenuates left ven-tricular hypertrophy induced pressure overload via its function of antioxidation and anti-inflammatory.