Resveratrol is a kind of iPolyphenols widely existing in herbal medicine. Here we aim to investigate whether resveratrol can reduce the degree of myocardial ischemia/reperfusion (IR) injury and inhibit the development of oxidative stress, and elucidate the molecular mechanism of resveratrol in protecting myocardial cells. The primary rat cardiomyocytes were used to establish an ischemia/reperfusion model in vitro, and a series of routine biochemical experiments were conducted to explore the antioxidant and anti-apoptotic effects of resveratrol in myocardial ischemia-reperfusion injury. Compared with that of the simulated ischemia-refusion (SIR) group, cell viability in the SIR and resveratrol co-treatment groups increased significantly (P < 0.001), the release of lactate dehydrogenase (LDH) and creatine kinase MB (CKMB) decreased, the positive rate of reactive oxygen species (ROS) in cardiomyocytes decreased, and the concentration of catalase and glutathione peroxidase increased significantly (P < 0.001). Besides, resveratrol can activate PI3K/AKT signaling pathway. PI3K siRNA can inhibit the PI3K/AKT signaling mediated by resveratrol. The addition of resveratrol can significantly increase the activity of mitochondrial superoxide dismutase (SOD) and reduce the malondialdehyde (MDA), which indicates that the oxidative damage of mitochondria induced by resveratrol was significantly weakened. The mitochondrial functional changes induced by resveratrol can be reversed by PI3K siRNA. In conclusion, our study shows that resveratrol can reduce ROS in cardiomyocytes by PI3K/AKT signaling pathway activation, and effectively inhibit the apoptosis of cardiomyocytes, thus having a direct protective effect on cardiomyocytes under SR.

白藜芦醇是一种广泛存在于草药中的iPolyphenols。在此我们旨在研究白藜芦醇是否可以减轻心肌缺血/再灌注（IR）损伤程度并抑制氧化应激的发展，并阐明白藜芦醇保护心肌细胞的分子机制。以大鼠原代心肌细胞体外建立缺血/再灌注模型，并进行一系列常规生化实验，探讨白藜芦醇在心肌缺血再灌注损伤中的抗氧化和抗凋亡作用。与模拟缺血再灌注（SIR）组相比，SIR和白藜芦醇联合治疗组的细胞活力显着增加（P < 0.001），乳酸脱氢酶（LDH）和肌酸激酶MB（CK）的释放明显增加（P < 0.001）。MB）降低，心肌细胞活性氧（ROS）阳性率降低，过氧化氢酶和谷胱甘肽过氧化物酶浓度显着升高（P < 0.001）。此外，白藜芦醇可以激活PI3K/AKT信号通路。PI3K siRNA 可以抑制白藜芦醇介导的 PI3K/AKT 信号传导。白藜芦醇的加入能显着提高线粒体超氧化物歧化酶（SOD）的活性，降低丙二醛（MDA），说明白藜芦醇对线粒体的氧化损伤明显减弱。白藜芦醇诱导的线粒体功能变化可以被 PI3K siRNA 逆转。综上所述，我们的研究表明，白藜芦醇可以通过激活PI3K/AKT信号通路降低心肌细胞内的ROS，有效抑制心肌细胞的凋亡，