人参皂甙 Rd 通过 PI3K/Akt 信号通路抑制炎症和细胞凋亡,减轻心肌缺血再灌注损伤

Yuanping Wang, Jiading Zheng, Xieyang Xiao, Cailing Feng, Yinghong Li, Hui Su, Ding Yuan, Qinghai Wang, Peihong Huang, Lili Jin
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引用次数: 0

摘要

心肌缺血/再灌注(I/R)损伤是导致全球死亡的主要原因。人参皂甙 Rd(GRd)具有保护心脏的特性,但其对心肌缺血再灌注损伤的疗效和作用机制尚未明确。本研究将 GRd 作为一种有效的心肌 I/R 损伤治疗药物进行研究。研究人员利用氧-葡萄糖剥夺和再灌注(OGD/R)以及冠状动脉左前降支(LAD)结扎术在体外和体内建立了心肌I/R损伤模型。在体内,GRd能明显缩小心肌梗死面积和心肌损伤指标,改善心肌I/R损伤小鼠的心功能。在体外,GRd能增强细胞活力,保护H9c2大鼠心肌母细胞免受OGD诱导的损伤。网络药理学分析预测了 GRd 治疗心肌 I/R 损伤的 48 个潜在靶点。GO和KEGG富集分析表明,GRd的心脏保护作用与PI3K/Akt信号通路介导的炎症和细胞凋亡密切相关。此外,GRd减轻了体内炎症和心肌细胞凋亡,抑制了OGD/R诱导的心肌细胞凋亡和炎症。GRd还增加了PI3K和Akt的磷酸化,表明PI3K/Akt通路被激活,而PI3K抑制剂LY294002阻断了GRd诱导的对OGD/R诱导的H9c2细胞凋亡和炎症的抑制。GRd在体内和体外对心肌I/R损伤的治疗作用主要依赖于PI3K/Akt通路的激活来抑制炎症和心肌细胞凋亡。这项研究为将 GRd 用作心血管药物提供了新的证据。
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Ginsenoside Rd Attenuates Myocardial Ischemia/Reperfusion Injury by Inhibiting Inflammation and Apoptosis through PI3K/Akt Signaling Pathway

Myocardial ischemia/reperfusion (I/R) injury is the leading cause of death worldwide. Ginsenoside Rd (GRd) has cardioprotective properties but its efficacy and mechanism of action in myocardial I/R injury have not been clarified. This study investigated GRd as a potent therapeutic agent for myocardial I/R injury. Oxygen-glucose deprivation and reperfusion (OGD/R) and left anterior descending (LAD) coronary artery ligation were used to establish a myocardial I/R injury model in vitro and in vivo. In vivo, GRd significantly reduced the myocardial infarct size and markers of myocardial injury and improved the cardiac function in myocardial I/R injury mice. In vitro, GRd enhanced cell viability and protected the H9c2 rat cardiomyoblast cell line from OGD-induced injury GRd. The network pharmacology analysis predicted 48 potential targets of GRd for the treatment of myocardial I/R injury. GO and KEGG enrichment analysis indicated that the cardioprotective effects of GRd were closely related to inflammation and apoptosis mediated by the PI3K/Akt signaling pathway. Furthermore, GRd alleviated inflammation and cardiomyocyte apoptosis in vivo and inhibited OGD/R-induced apoptosis and inflammation in cardiomyocytes. GRd also increased PI3K and Akt phosphorylation, suggesting activation of the PI3K/Akt pathway, whereas LY294002, a PI3K inhibitor, blocked the GRd-induced inhibition of OGD/R-induced apoptosis and inflammation in H9c2 cells. The therapeutic effect of GRd in vivo and in vitro against myocardial I/R injury was primarily dependent on PI3K/Akt pathway activation to inhibit inflammation and cardiomyocyte apoptosis. This study provides new evidence for the use of GRd as a cardiovascular drug.

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