Gatrodin is an active compound with cardio-protective potentials. In the current study, the mechanism underlying the effects of gastrodin was explored. Myocardial infarction was induced and handled with gastrodin. The role of miR-30a-5p and its downstream effector, ATG5, in the cardio-protective effects of gastrodin was verified. Gastrodin induced the dys-expresseion of 72 miRs in oxygen/glucose deprivation (OGD) cardiomyocytes and miR-30a-5p was selected as the potential therapeutic target. Gastrodin increased viability and suppressed autophagy in OGD cardiomyocytes, which was associated with the induction of miR-30a-5p and deactivation of ATG5. In rat models, gastrodin attenuated structure deterioration and dysfunction in heart, and suppressed autophagy. At molecular level, miR-30a-5p was induced and ATG5 were down-regulated. After the suppression of miR-30a-5p or the overexpression of ATG5, the cardio-protective effects of gastrodin were compromised. Gastrodin induced the expression of miR-30a-5p, which contributed to the attenuation of autophagy in infarcted heart tissues.

Gatrodin 是一种具有心脏保护潜力的活性化合物。在当前的研究中，探索了天麻素作用的潜在机制。用天麻素诱导和处理心肌梗塞。验证了 miR-30a-5p 及其下游效应子 ATG5 在天麻素的心脏保护作用中的作用。天麻素诱导氧/糖剥夺 (OGD) 心肌细胞中 72 个 miR 的表达异常，miR-30a-5p 被选为潜在的治疗靶点。天麻素增加 OGD 心肌细胞的活力并抑制自噬，这与 miR-30a-5p 的诱导和 ATG5 的失活有关。在大鼠模型中，天麻素可减轻心脏结构退化和功能障碍，并抑制自噬。在分子水平上，miR-30a-5p 被诱导，ATG5 被下调。miR-30a-5p 抑制或 ATG5 过表达后，天麻素的心脏保护作用受到损害。天麻素诱导 miR-30a-5p 的表达，这有助于减弱梗塞心脏组织中的自噬。