重组人促红细胞生成素对压力超负荷大鼠左室肥厚的抑制作用

Effect of rhEPO on left ventricular hypertrophy induced by pressure-overload

关键词:  心室肥厚  压力超负荷  氧化应激  炎症  促红细胞生成素

Key words:  [Key words]　ventricular hypertrophy  pressure overload  oxidative stress  inflammation  erythropoietin

摘要:

[摘要]　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。

Abstract:

[Abstract]　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-α in myocardium were detected respectively.　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-α decreased, SOD level improved in myocardium (P<0.01).　Conclusion　RhEPO could attenuates left ventricular hypertrophy induced pressure overload via its function of antioxidation and anti-inflammatory.