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观察血管紧张素Ⅱ（ＡｎｇⅡ）对心肌肌浆网Ｃａ２＋，Ｍｇ２＋－ＡＴＰａｓｅ基因（ＳＥＲＣＡ２ａ）转录调节的影响，评价ＤＭＰ８１１对此效应的干预作用．６周龄雄性ＳＤ大鼠随机分为３组，每组６只．组１：生理盐水输注；组２：ＡｎｇⅡ输注＋ＤＭＰ８１１管饲（３ｍｇ·ｄ－１·ｋｇ－１）；组３：ＡｎｇⅡ输注（２００ｎｇ·ｍｉｎ－１·ｋｇ－１．１周后称其体重，取心脏并称重，提取心脏总ＲＮＡ后采用Ｎｏｒｔｈｅｒｎｂｌｏｔ的方法检测ＳＥＲ－ＣＡ２ａ的转录水平，采用ＲＴ－ＰＣＲ检测ＡｎｇⅡ１型受体（ＡＴ１）ｍＲＮＡ水平．实验后，组３心重（ＣＷ）、心重／体重（Ｃ／Ｂ）、ＡＴ１受体转录水平均高于组１（分别增加４．７±０．４％，４．９±０．９％和２４．７±３．５％；Ｐ＜０．０１），而ＳＥＲＣＡ２ａ基因转录水平显著低于组１（降低２０．１±３．０％，Ｐ＜０．０１），并且ＳＥＲＣＡ２ａｍＲＮＡ水平与ＡＴ１受体ｍＲＮＡ水平呈负相关（ｒ＝－０．７４，Ｐ＜０．０１）．ＡｎｇⅡ导致的上述改变能被ＤＭＰ８１１完全阻断．ＡｎｇⅡ通过其Ⅰ型受体的介导，诱导了ＳＥＲＣＡ２ａ的转录下调
To observe the effect of angiotensin Ⅱ (AngⅡ) on the transcriptional regulation of Ca2 + and Mg2 + -ATPase genes (SERCA2a) in cardiac sarcoplasmic reticulum and evaluate the effect of DMP811 on this effect. Six-week-old male Sprague-Dawley rats were randomly divided into 3 groups with 6 rats in each group. Group 1: saline infusion; Group 2: Ang Ⅱ infusion + DMP811 tube feeding (3 mg · d-1 · kg-1); Group 3: AngⅡ infusion (200 ng · min-1 · kg-1.1 weeks later The heart weight was measured and the heart was weighed. The total RNA of heart was extracted and the transcription level of SER-CA2a was detected by Northern blot. The mRNA expression of AngⅡ receptor (AT1) was detected by RT- , Heart / body weight (C / B) and AT1 receptor were higher than those in group 1 (increased by 4.7 ± 0.4%, 4.9 ± 0.9% and 24.7 ± 3.5% respectively; (P <0.01), while SERCA2a gene transcription was significantly lower than that of group 1 (20.1 ± 3.0%, P <0.01), and the level of SERCA2amRNA was negatively correlated with AT1 receptor mRNA level (r = -0.74, P <0.01). AngⅡ induced the above changes Can be completely blocked by DMP811. AngⅡ induces the down-regulation of SERCA2a transcription through its type I receptor