Medicinal Plant Research 2025, Vol.15, No.5, 233-243 http://hortherbpublisher.com/index.php/mpr 235 The synergistic effect among these components enhances the overall cardioprotective effect of S. miltiorrhiza extract. The interaction of its multiple components can improve blood circulation, reduce infarction area, and better maintain cardiac function in ischemic heart disease models (Wei et al., 2023; Mu et al., 2024; Qian et al., 2025). The latest research indicates that, the combined application of tanshinone I and salfanolic acid A, can exhibit a synergistic effect on vascular normalization, and tissue protection in ischemic models (Qian et al., 2025). This multi-target and multi-pathway mode of action is precisely the basis for S. miltiorrhiza to play a role in traditional medicine and modern cardiovascular treatment (Ye et al., 2023; Mu et al., 2024). 3 Pathophysiology of Myocardial Ischemic Injury and the Regulatory Role 3.1 Oxidative stress and cellular damage under S. miltiorrhiza intervention Myocardial ischemia leads to excessive reactive oxygen species (ROS) production and mitochondrial dysfunction, resulting in oxidative damage and cell death. Tanshinones, key lipophilic components of S. miltiorrhiza, have been shown to attenuate ROS generation, preserve mitochondrial integrity, and reduce oxidative injury in ischemic heart models, thereby protecting cardiomyocytes from ischemia-reperfusion damage (Huang et al., 2023; Zhong et al., 2023). Hydrophilic constituents, like salvianolic acid B, exert potent antioxidant effects by scavenging free radicals and activating the Nrf2 signaling pathway, which upregulates endogenous antioxidant defenses (Hu et al., 2019; Tao et al., 2019; Shen et al., 2022). This reduces lipid peroxidation, ferroptosis, and apoptosis in cardiomyocytes following ischemic injury. 3.2 Inflammation and apoptosis modulated by S. miltiorrhiza S. miltiorrhiza extract can inhibit the activation of the NF-κB pathway, and down-regulate the levels of pro-inflammatory cytokines, like TNF-α, IL-1β and IL-6, thereby alleviating the inflammatory response after myocardial ischemia (Duan et al., 2023; Huang et al., 2023; Shan et al., 2024). This anti-inflammatory effect is mainly mediated through the TLR4/NF-κB and NLRP3 inflammasome pathways. Meanwhile, S. miltiorrhiza reduces the apoptotic level of cardiomyocytes, by activating survival signaling pathways (e.g., Akt/ERK1/2/Nrf2, JAK2/STAT3), and inhibiting pro-apoptotic factors, thereby increasing the survival rate of myocardium after ischemic injury (Huang et al., 2023; Zhong et al., 2024). 3.3 Hemodynamic dysfunction and endothelial injury improved by S. miltiorrhiza Ischemic injury can weaken endothelial function and vasodilation ability. S. miltiorrhiza improves vasodilation and restores endothelial function, by enhancing endothelial nitric oxide synthase (eNOS) activity, and increasing nitric oxide (NO) production, which is crucial for maintaining myocardial perfusion (Huang et al., 2023; Wu et al., 2024). S. miltiorrhiza and its active ingredients also can promote angiogenesis, protect microvascular integrity, and improve microcirculation disorders in ischemic myocardium. This process is partially achieved by up-regulating VEGF and related pathways (Zhang et al., 2023). 4 Cardioprotective Effects of Salvia miltiorrhiza 4.1 Antioxidant and free radical scavenging effects S. miltiorrhiza extract and its active components, like tanshinone and salvianate, can significantly enhance the activity of endogenous antioxidant enzymes in myocardial tissue, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX). In animal models and clinical studies, this upregulation effect has been consistently observed, thereby improving the clearance ability of reactive oxygen species (ROS), and protecting cardiomyocytes from oxidative damage during ischemia (Chang et al., 2016; Ren et al., 2019; Li et al., 2025). S. miltiorrhiza treatment can also reduce the generation of lipid peroxidation products, such as malondialdehyde (MDA) and thiobarbituric acid reactants (TBARS), which are important markers of oxidative membrane damage. This effect effectively maintains the integrity of myocardial cell membranes, and limits the injury range caused by ischemia (Cheng et al., 2021). The inhibition of lipid peroxidation is closely related to the upregulation of antioxidant enzyme activity, and the direct free radical scavenging effect of S. miltiorrhiza components.
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