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目的探讨表没食子儿茶素没食子酸酯(EGCG)对腹主动脉缩窄大鼠心肌肥厚的影响及可能机制。方法 30只SD大鼠随机均分为腹主动脉缩窄组(A组)、腹主动脉缩窄+EGCG组(B组)和假手术组(C组)。4周后,计算左室重量/体重(LVW/BW)比值以判断大鼠心肌肥厚程度,Western blot法检测双特异性酪氨酸磷酸化调控激酶1A(Dyrk1A)和可变剪接因子(ASF)蛋白表达,RT-PCR法检测钙调素依赖蛋白激酶Ⅱδ(CaMKⅡδ)mRNA表达。结果与C组相比,A组大鼠LVW/BW升高,心肌中Dyrk1A蛋白及CaMKⅡδA、B亚型mRNA表达增加,ASF蛋白及CaMKⅡδC亚型mRNA表达下降(P<0.05);而B组能明显逆转A组上述指标的变化(P<0.05)。结论 EGCG可通过调控Dyrk1A-ASF-CaMKⅡδ可变剪接的信号通路预防腹主动脉缩窄大鼠心肌肥厚的发生。
Objective To investigate the effect of epigallocatechin gallate (EGCG) on cardiac hypertrophy in abdominal aorta and its possible mechanism. Methods Thirty SD rats were randomly divided into abdominal aorta constriction group (A group), abdominal aorta constriction group (EGCG group) and sham operation group (C group). After 4 weeks, the ratio of left ventricular mass to body weight (LVW / BW) was calculated to determine the degree of myocardial hypertrophy in rats. Bispecific tyrosine phosphorylation regulatory kinase 1A (Dyrk1A) and alternative splicing factor (ASF) The expression of CaMKⅡδ mRNA was detected by RT-PCR. Results Compared with group C, the LVW / BW of group A was increased, the expression of Dyrk1A protein and CaMKⅡδA, B subtype increased, while the expression of ASF protein and CaMKⅡδC subtype decreased (P <0.05); while group B Obvious reversal of the above indicators in group A changes (P <0.05). Conclusion EGCG can prevent cardiac hypertrophy in rats with abdominal aorta stenosis by regulating the alternative splicing of Dyrk1A-ASF-CaMKⅡδ.