Protective effect of hyperoside on heart failure rats via attenuating myocardial apoptosis and inducing autophagy

Heart failure (HF) is one of the most severe heart conditions, which lacks effective therapies. Therefore, it is necessary to develop more efficient drugs for HF. In this study, we investigated the cardioprotective effects of hyperoside against the pathological progression of HF. Thoracic aortic constriction (TAC) was performed to induce HF in rats. Hyperoside treatment improved cardiac function, decreased cardiomyocyte cross-sectional area and heart weight to body weight (HW/BW) ratio in HF rats. Moreover, hyperoside administration repressed apoptosis as evidenced by changing apoptosis-related protein levels, and promoted autophagy in TAC rats and angiotensin II (AngII)-induced H9C2 cells. Inhibition of autophagy by 3-methyladenine (3-MA) attenuated the beneficial effect of hyperoside against apoptosis in H9C2 cells. In summary, these data confirm that hyperoside effectively alleviates HF via suppressing apoptosis and inducing autophagy, which provides evidence that hyperoside may serve as a promising natural drug for treating HF. Hyperoside (Hyp) protects against heart failure via attenuating myocardial apoptosis and inducing autophagy

心力衰竭（Heart Failure, HF）是最为严重的心脏疾病之一，目前尚无有效的治疗手段，因此开发针对HF的高效药物具有重要意义。本研究探讨了金丝桃苷（hyperoside）对心力衰竭病理进展的心脏保护作用。研究通过对大鼠施行胸主动脉缩窄术（Thoracic Aortic Constriction, TAC）以构建心力衰竭模型。结果显示，金丝桃苷干预可改善心力衰竭大鼠的心脏功能，缩小心肌细胞横截面积，并降低心脏重量与体重比值（HW/BW）。此外，通过检测凋亡相关蛋白的表达变化证实，金丝桃苷给药可抑制细胞凋亡，同时在TAC模型大鼠及血管紧张素Ⅱ（Angiotensin II, AngII）诱导的H9C2细胞中促进自噬。使用3-甲基腺嘌呤（3-Methyladenine, 3-MA）抑制自噬，可削弱金丝桃苷对H9C2细胞凋亡的保护作用。综上，本研究数据证实金丝桃苷可通过抑制细胞凋亡、诱导自噬有效缓解心力衰竭，为其作为极具潜力的天然抗心力衰竭药物提供了实验依据。金丝桃苷（Hyp）可通过减轻心肌细胞凋亡、诱导自噬发挥抗心力衰竭作用。