Medicinal Plant Research 2025, Vol.15, No.5, 214-223 http://hortherbpublisher.com/index.php/mpr 217 apoptosis of nerve cells, promoting cerebral angiogenesis, and activating signaling pathways, such as AKT/mTOR and PINK1/Parkin (Figure 1). Z-ligustilide also can protect neurons by maintaining mitochondrial health, and reducing oxidative damage (Shen et al., 2024). Figure 1 Mechanisms of A. sinensis and its compounds in the treatment of cerebrovascular diseases (Adopted from Chen et al., 2024) Image caption: The figure illustrates how the polysaccharides, volatile oils, and key active components of Angelica sinensis exert their effects by inhibiting inflammatory responses, reducing oxidative stress, suppressing neuronal apoptosis, promoting cerebrovascular angiogenesis, and activating signaling pathways such as PI3K/Akt/mTOR and PINK1/Parkin. This indicates that A. sinensis can comprehensively improve ischemic brain injury, alleviate vascular dementia, and protect brain cells, highlighting its multi-target therapeutic potential in the prevention and treatment of cerebrovascular diseases (Adapted from Chen et al., 2024) In ischemic events, A. sinensis can maintain the integrity of the blood-brain barrier (BBB) through reducing oxidative and inflammatory damage to endothelial cells. Especially Z-ligustilide, which can inhibit vascular endothelial fibrosis, promote angiogenesis and protect the BBB, thereby jointly limiting secondary brain injury after stroke (Cheng et al., 2017; Shen et al., 2024). Experimental studies have shown that, A. sinensis extract can upregulate the expression of vascular endothelial growth factor A (VEGF-A) and von Willebrand factor (vWF), thereby promoting vascular repair and maintaining BBB stability (Cheng et al., 2017; 2020). 4.2 Regulation of neuroinflammation A. sinensis can regulate the activation of microglia, and the activation of microglia is a key driver of neuroinflammation in cerebral ischemia. Human participation in the combined application of A. sinensis, can inhibit the activation of NLRP3 inflammasome and pyroptosis of microglia, thereby reducing neuroinflammatory injury and promoting neuronal survival (Hu et al., 2020). Z-ligustilide can also inhibit the activation of microglia and inflammasome pathways, further exerting neuroprotective effects (Shen et al., 2024). A. sinensis and its active components, can inhibit the release of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α, etc.), and down-regulate the NF-κB signaling pathway, thereby reducing neuroinflammatory responses, and improving prognosis in ischemic brain injury (Han et al., 2021; Xu et al., 2021; Chen et al., 2024). These anti-inflammatory effects are one of the core mechanisms, by which A. sinensis limits secondary neuronal damage and promotes recovery.
RkJQdWJsaXNoZXIy MjQ4ODYzNA==