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首页> 外文期刊>Cardiovascular therapeutics >Downregulation of miR-21 is Involved in Direct Actions of Ursolic Acid on the Heart: Implications for Cardiac Fibrosis and Hypertrophy
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Downregulation of miR-21 is Involved in Direct Actions of Ursolic Acid on the Heart: Implications for Cardiac Fibrosis and Hypertrophy

机译：miR-21的下调涉及熊果酸对心脏的直接作用：对心脏纤维化和肥大的影响。

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Purpose: Myocardial fibrosis contributes to cardiac remodeling and loss of cardiac function in myocardial infarction and heart failure. This study used in vitro and in vivo models to examine the effects of ursolic acid (UA) on myocardial fibrosis and to explore its potential mechanism. Methods: Transverse aortic constriction (TAC) surgery was performed in mice to induce cardiac hypertrophy and fibrosis. UA was orally administered 1 week prior to TAC. Two weeks after TAC, myocardial pathology was detected using Masson's trichrome staining and transmission electron microscopy, and heart-to-body weight ratio was measured. For in vitro studies, cultured cardiac fibroblasts were treated with serum in the presence or absence of UA. The relative levels of miR-21 and p-ERK/ERK, collagen content and cell viability were measured. Results: Ursolic acid attenuated pathological cardiac hypertrophy and myocardial fibrosis in vivo induced by TAC. Downregulation of miR-21 and p-ERK/ERK were observed in myocardial fibroblasts treated with UA in a dose-dependent manner compared with the control group both in vitro and in vivo. Conclusions: Our study demonstrates that UA can inhibit myocardial fibrosis both in vitro and in vivo, and the effects of UA on myocardial fibrosis may be due to the inhibition of miR-21/ERK signaling pathways.
机译：目的：心肌纤维化有助于心肌梗塞和心力衰竭的心脏重塑和心脏功能丧失。这项研究使用体外和体内模型研究了熊果酸（UA）对心肌纤维化的影响，并探讨了其潜在机制。方法：对小鼠进行横断主动脉缩窄（TAC）手术，以诱发心脏肥大和纤维化。 TAC前1周口服UA。 TAC后两周，使用Masson的三色染色和透射电子显微镜检测心肌病理，并测量心体重比。对于体外研究，在存在或不存在UA的情况下，用血清处理培养的心脏成纤维细胞。测量了miR-21和p-ERK / ERK的相对水平，胶原蛋白含量和细胞活力。结果：熊果酸可减轻TAC体内的病理性心肌肥大和心肌纤维化。与对照组相比，在UA处理后的心肌成纤维细胞中，与对照组相比，miR-21和p-ERK / ERK均下调。结论：我们的研究表明，UA可以在体外和体内抑制心肌纤维化，并且UA对心肌纤维化的影响可能是由于miR-21 / ERK信号通路的抑制所致。

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