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作 者:贾皓[1] 余小平[1] 彭晓莉[1] 程道梅[1]
出 处:《成都医学院学报》2011年第3期205-210,共6页Journal of Chengdu Medical College
基 金:国家自然科学基金(No:30972462);教育部新世纪优秀人才支持计划(No:NECT-08-0901);教育部重点项目(No:208123)
摘 要:目的探讨表没食子儿茶素没食子酸酯(Epigallocathechin-3Gallate,EGCG)是否能够抑制压力超负荷导致的心肌肥厚。方法心肌肥厚模型通过腹主动脉收缩术(abdominal aortic constriction,AC)实现。结果手术后3周,HW/BW在AC组比sham组增加了34%。EGCG将AC组的心脏重量的增加缩小了69%。EGCG抑制的心肌肥厚的减少与肥厚心肌细胞尺寸及纤维化的缩小相关联。超声波心动图数据显示EGCG改善了增加的左心室收缩期尺寸及恶化的收缩机能。结论 EGCG可以预防压力超负荷导致的左心室肥厚的发展。Objective To investigate whether Epigallocatechin-3 gallate(EGCG)supplementation could reduce in vivo pressure overloadmediated cardiac hypertrophy.Methods Cardiac hypertrophy was induced by suprarenal transverse abdominal aortic constriction(AC) in rats.Results Three weeks after AC surgery,heart to body weight ratio increased in the AC group by 34% compared to the sham group.EGCG administration suppressed the load-induced increase in heart weight by 69%.Attenuation of cardiac hypertrophy by EGCG was associated with attenuation of the increase in myocyte cell size and fibrosis induced by aortic constriction.Despite abolition of hypertrophy by EGCG,transstenotic pressure gradients did not change.Echocardiogram revealed that increased left ventricular systolic dimensions and deteriorated systolic function were relieved by EGCG.Conclusion EGCG prevents the development of left ventricular concentric hypertrophy by pressure overload.
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