Mounting evidences indicate that autophagy is an essential homeostatic mechanism to maintain the global cardiac structure function. Sophocarpine (SOP), a major bioactive compound derived from the natural plant Sophora flavescens. However, the role of SOP in cardiac hypertrophy remain to be fully elucidated. In the present study, we tested the hypothesis that SOP protects against Ang II–induced cardiac hypertrophy by mediating the regulation of autophagy. The results demonstrated that SOP attenuated the Ang II–induced cardiac hypertrophy, as assessed by measurements of echocardiography parameters, the ratios of heart weight/body weight and left ventricle weight/body weight, histopathological staining, cross-sectional cardiomyocyte area, and the expression levels of cardiac hypertrophic markers. The anti-hypertrophic effect of SOP was mediated by activating autophagy-related pathway, as revealed by reversal of the increased autophagy marker protein expression. These findings reveal a novel mechanism of SOP attenuating cardiac hypertrophy via activating autophagy-related signaling pathways.

越来越多的证据表明自噬是维持整体心脏结构功能的重要稳态机制。槐果碱 (SOP)，一种源自天然植物苦参的主要生物活性化合物. 然而，SOP 在心脏肥大中的作用仍有待充分阐明。在本研究中，我们检验了 SOP 通过调节自噬来防止 Ang II 诱导的心脏肥大的假设。结果表明，通过测量超声心动图参数、心脏重量/体重和左心室重量/体重的比率、组织病理学染色、横截面心肌细胞面积和表达来评估，SOP 减轻了 Ang II 诱导的心脏肥大心肌肥厚标志物的水平。SOP 的抗肥大作用是通过激活自噬相关通路介导的，正如自噬标记蛋白表达增加的逆转所揭示的那样。