Medicinal Plant Research 2025, Vol.15, No.5, 233-243 http://hortherbpublisher.com/index.php/mpr 236 4.2 Anti-inflammatory and anti-apoptotic effects S. miltiorrhiza and its active components, especially tanshinone IIA and salvianolic acids, can inhibit the activation of the NF-κB signaling pathway, and down-regulate the expression of pro-inflammatory cytokines, like TNF-α, IL-1β and IL-6. This anti-inflammatory effect has been verified in both in vitro and in vivo models of myocardial ischemia, manifested as a reduction in inflammatory cell infiltration and tissue damage (Ren et al., 2019; Wei et al., 2023; Wu et al., 2024; Li et al., 2025). As Li et al. (2025) found, the active components of S. miltiorrhiza, such as tanshenone and tanshenic acid, exert anti-fibrotic effects through multiple mechanisms, containing inhibiting ventricular remodeling, regulating autophagy, promoting extracellular matrix degradation, anti-inflammation, inhibiting oxidative stress and cardiomyocyte apoptosis (Figure 1). Figure 1 Mechanism of Salvia miltiorrhiza Bunge in the treatment of MF (①SM inhibitsMFby downregulating TGF-β1, Smad2/3, and their phosphorylation levels; ②SM inhibits MF by downregulating the phosphorylation levels of PI3K, Akt, and mTOR proteins; ③SM inhibits MF by downregulating the expression of TLR4 and the activation of downstream TAK1 and NF-κB; ④SM inhibits apoptosis and MF by upregulating the expression of Bax, Caspase-3, Caspase-9, and cytochrome C, and downregulating Bcl-2 protein; ⑤SM regulates the TIMP-1/MMPs pathway to inhibit MF by downregulating the expression of MMP2 and MMP9, and upregulating TIMP-1 expression; ⑥SM regulates the Nrf2/HO-1 signaling pathway to inhibit MF by upregulating the expression of antioxidant proteins such as Nrf2 and HO-1) (Adopted from Li et al., 2025) Besides, S. miltiorrhiza extract regulates the apoptotic pathway by increasing the expression of anti-apoptotic protein Bcl-2 and reducing the level of pro-apoptotic protein Bax, thereby reducing cardiomyocyte apoptosis and improving cell survival rate after ischemic injury (Guo et al., 2020; Hung et al., 2020; Jung et al., 2020; Zhang et al., 2023). This cytoprotective mechanism achieved by regulating the Bcl-2/Bax ratio is an important link for S. miltiorrhiza to exert cytoprotective effects in ischemic myocardium. 4.3 Improvement of hemodynamics S. miltiorrhiza can enhance the activity of endothelial nitric oxide synthase (eNOS), and the production of nitric oxide (NO), promote vasodilation and improve vascular function. This effect is crucial for restoring blood flow to ischemic myocardium, and has been confirmed by preclinical and clinical studies (Chang et al., 2016; Wang et al., 2017; Luo et al., 2023; Zhang et al., 2025). By improving endothelial function and microcirculation, S. miltiorrhiza can increase coronary blood flow and myocardial perfusion, which helps maintain cardiac function, and reduce infarction area in ischemic heart disease models (Mu et al., 2017; Ren et al., 2019; Cheng et al., 2021). This hemodynamic improvement is also associated with better recovery of left ventricular function, and a slower progression of heart failure.
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