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首页> 外文期刊>American Journal of Physiology >All-trans retinoic acid prevents development of cardiac remodeling in aortic banded rats by inhibiting the renin-angiotensin system.
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All-trans retinoic acid prevents development of cardiac remodeling in aortic banded rats by inhibiting the renin-angiotensin system.

机译：全反式维甲酸通过抑制肾素-血管紧张素系统，防止主动脉带状大鼠心脏重构的发展。

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摘要

This study was designed to determine the effect of all-trans retinoic acid (RA) on the development of cardiac remodeling in a pressure overload rat model. Male Sprague-Dawley rats were subjected to sham operation and the aortic constriction procedure. A subgroup of sham control and aortic constricted rats were treated with RA for 5 mo after surgery. Pressure-overloaded rats showed significantly increased interstitial and perivascular fibrosis, heart weight-to-body weight ratio, and gene expression of atrial natriuretic peptide and brain natriuretic peptide. Echocardiographic analysis showed that pressure overload induced systolic and diastolic dysfunction, as evidenced by decreased fractional shortening, ejection fraction, stroke volume, and increased E-to-E(a) ratio and isovolumic relaxation time. RA treatment prevented the above changes in cardiac structure and function and hypertrophic gene expression in pressure-overloaded rats. RA restored the ratio of Bcl-2 to Bax, inhibited cleavage of caspase-3 and -9, and prevented the decreases in the levels of SOD-1 and SOD-2. Pressure overload-induced phosphorylation of ERK1/2, JNK, and p38 was inhibited by RA, via upregulation of mitogen-activated protein kinase phosphatase (MKP)-1 and MKP-2. The pressure overload-induced production of angiotensin II was inhibited by RA via upregulation of expression of angiotensin-converting enzyme (ACE)2 and through inhibition of the expression of cardiac and renal renin, angiotensinogen, ACE, and angiotensin type 1 receptor. Similar results were observed in cultured neonatal cardiomyocytes in response to static stretch. These results demonstrate that RA has a significant inhibitory effect on pressure overload-induced cardiac remodeling, through inhibition of the expression of renin-angiotensin system components.
机译：这项研究旨在确定全反式维甲酸（RA）对压力超负荷大鼠模型心脏重构发展的影响。对雄性Sprague-Dawley大鼠进行假手术和主动脉收缩程序。假对照组和主动脉缩窄大鼠的亚组在手术后用RA治疗5个月。压力超负荷的大鼠显示间质和血管周纤维化明显增加，心脏重量与体重之比，以及心钠素和脑钠素的基因表达。超声心动图分析表明，压力超负荷可引起收缩和舒张功能障碍，这可通过缩短分数缩短，射血分数，中风量以及增加E-E（a）比和等容舒张时间来证明。 RA治疗可预防压力超负荷大鼠的上述心脏结构和功能以及肥大基因表达的上述变化。 RA恢复了Bcl-2与Bax的比率，抑制了caspase-3和-9的裂解，并阻止了SOD-1和SOD-2的水平降低。 RA通过上调丝裂原活化的蛋白激酶磷酸酶（MKP）-1和MKP-2抑制了压力超负荷诱导的ERK1 / 2，JNK和p38磷酸化。 RA通过上调血管紧张素转化酶（ACE）2的表达，并通过抑制心脏和肾脏肾素，血管紧张素原，ACE和血管紧张素1型受体的表达来抑制压力超负荷诱导的血管紧张素II的产生。在培养的新生儿心肌细胞对静态拉伸的反应中观察到了相似的结果。这些结果表明，RA通过抑制肾素-血管紧张素系统成分的表达，对压力超负荷引起的心脏重塑具有显着的抑制作用。

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