Medicinal Plant Research 2025, Vol.15, No.5, 214-223 http://hortherbpublisher.com/index.php/mpr 218 4.3 Neural repair and regeneration A. sinensis extract can activate neuronutrition-related signaling pathways, including the p38 MAPK/CREB/BDNF pathway, promoting the expression of brain-derived neurotrophic factor (BDNF) and other growth factors, which are crucial for the survival and repair of neurons after ischemic injury. It is helpful for neurogenesis and functional recovery (Shen et al., 2016; Cheng et al., 2017; 2020). By up-regulating BDNF and related signals, A. sinensis enhance synaptic plasticity and promote neural regeneration, improving cognitive and neurological functional outcomes after cerebral ischemia (Cheng et al., 2020; Zhao et al., 2023). The volatile oil components of A. sinensis have also been proven to increase the expression of proteins related to synaptic plasticity, further supporting the recovery of cognitive function (Zhao et al., 2023). 5 Mechanistic Pathways of Action inAngelica sinensis 5.1 PI3K/Akt and MAPK pathways A. sinensis and its active components, like polysaccharides and ferulic acid, could activate the PI3K/Akt pathway, which plays a key role in promoting cell survival and inhibiting apoptosis. This activation enhance the expression of anti-apoptotic proteins, such as Bcl-2, and reduce the levels of pro-apoptotic markers (e.g., Bax, caspase-3), thereby protecting cardiovascular and liver tissue cells from oxidative and inflammatory damage (Du et al., 2023; Lu and Wang, 2025). In ischemic injury and oxidative stress models, PI3K/Akt signaling mediate cell protection and promote tissue repair (Niu et al., 2018; Lu and Wang, 2025). When returned, it can exert anti-inflammatory and anti-apoptotic effects by regulating the MAPK pathway, containing p38 MAPK. MAPK signal activation can regulate the expression of inflammatory mediators, enhance the resistance of cells to stress-induced apoptosis, and achieve protection for blood vessels and the nervous system (Chen et al., 2022; Huang et al., 2023). In the context of antifungal and angiogenic research, MAPK activation has also been confirmed to mediate cell survival and adaptability (Gao et al., 2023). 5.2 Nrf2/HO-1 and antioxidant regulation ASP can promote the nuclear translocation of Nrf2, which is a core regulatory factor in antioxidant defense. This process can up-regulate the expression of multiple antioxidant genes, including those encoding superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX), thereby reducing oxidative stress and alleviating cell damage (Du et al., 2023; Ren et al., 2025). The activation of Nrf2 is regarded as a key link for ASP, to exert antioxidant and cytoprotective effects in various tissues. The downstream target of Nrf2, heme oxygenase-1 (HO-1), can also be upregulated by A. sinensis, thereby enhancing its vascular protective effect. HO-1 has anti-inflammatory, antioxidant and anti-apoptotic effects, can maintain vascular endothelial function, and reduce tissue damage in the cardiovascular and cerebrovascular systems (Ren et al., 2025). 6 Experimental Evidence in Cells and Animals of A. sinensis 6.1 Cell-based studies A. sinensis polysaccharide (ASP) and ferulic acid, have shown protective effects in various cell models. In endothelial cells and perivascular mesenchymal progenitor cells, ASP can alleviate oxidative stress, promote cell proliferation, and enhance differentiation potential (Niu et al., 2023). In HepG2 cells, ferulic acid improves ethanol induced injury, by regulating the AMPK/ACC and PI3K/AKT pathways, showing cell protective and metabolic regulatory effects (Lu and Wang, 2025). Different ASP grades at different root sites in IPEC-J2 cells, exhibited different anti-inflammatory and antioxidant activities. Some of these grades showed stronger protective effects against LPS-induced inflammation and oxidative stress (Zou et al., 2022). The results of cell experiments consistently indicated that, ASP and related extracts could down-regulate pro-inflammatory cytokines (IL-1β, IL-6, TNF-α, etc.), while up-regulating the levels of antioxidant enzymes (like SOD, CAT, GPX) (Zou et al., 2022; Niu et al., 2023). These effects are closely related to the inhibition of NF-κB
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