Retracted Article: Vitexin mitigates myocardial ischemia reperfusion-induced damage by inhibiting excessive autophagy to suppress apoptosis via the PI3K/Akt/mTOR signaling cascade

Abstract

Myocardial ischemia reperfusion (MI/R) injury is reported to induce apoptosis and autophagy of myocardial cells and contribute to adverse cardiovascular outcomes.

Scabiosa Genus: A Rich Source of Bioactive Metabolites

“…Although, herein we are disclosing the more recent in vivo studies, it is a surprise that this metabolite’s in vivo evaluation started in 1995 with a study of its antithyroid effects, concluding that can be used to prevent goiter [71]. The more recent studies include antimicrobial activity against Pseudomonas aeruginosa , for which the vitexin 19 activity was moderated [72], cardioprotective effects, which demonstrated that vitexin 19 mitigated myocardial ischemia reperfusion injury and suppressed apoptosis and autophagy in myocardium cells [73], and its protection of dopaminergic neurons, which suggests its use in Parkinson’s disease therapy [74].…”

Effect and mechanism of asiatic acid on autophagy in myocardial ischemia‑reperfusion injury <em>in&nbsp;vivo</em> and <em>in&nbsp;vitro</em>

“…During MIRI, the excessive accumulation of ROS results in increased phosphorylation of Bcl-2, disrupting the balance between Bcl-2 and beclin-1. The subsequent dissociation of the Bcl-2/beclin-1 complex causes the release of large quantities of beclin-1, which results in excessive autophagy and, possibly, autophagy-dependent cell death (25). Therefore, the balance between Bcl-2 and beclin-1 appears to underlie the activation of autophagy.…”

“…C57BL/6 mice were anesthetized with an intraperitoneal injection of 1% pentobarbital sodium (30 mg/kg) and fixed in the supine position ( 25 ). An oral tracheal tube was inserted and connected to an animal ventilator, and the limb-lead electrocardiogram was recorded.…”

“…Animal Center of Jiangsu Province (Nanjing, China)], weighing 20-25 g and aged 4-6 weeks, were given free access to food and water and were kept under 12:12 h light-dark cycles at room temperature with 40-60% humidity for 1 week for adaptation, after which time all mice were randomized and divided into three groups (n=10 per group) as follows (all treatments were performed once per day for 7 days): Sham operation group, pretreated with PBS for 7 days before the operation; MIRI group, pretreated with PBS for 7 days before the operation; and MIRI + AA group, pretreated with AA (100 mg/kg/day via oral gavage) for 7 days before the operation. C57BL/6 mice were anesthetized with an intraperitoneal injection of 1% pentobarbital sodium (30 mg/kg) and fixed in the supine position (25). An oral tracheal tube was inserted and connected to an animal ventilator, and the limb-lead electrocardiogram was recorded.…”

“…SOD activity and MDA content were measured as the decomposition products of lipid hydroperoxides. These are often used as indicators of oxidative damage to cells and tissues (25,29,30), and were used in the current in vitro study by SOD and MDA assay kits to detect the antioxidant performance of AA according to the manufacturer's protocol. In brief, the H9c2 cells were initially cultured at a density of 1x10 4 cells/well in 96-well plates at 37˚C.…”