This study focuses on the mechanism by which Danggui Shaoyao San(DSS) regulates hepatic fatty acid metabolism to promote ketone body production, transport, and utilization, thereby alleviating brain energy metabolism disorders in APP/PS1 mice and enhancing their cognitive abilities. Six SPF-grade 3-month-old male C57BL/6J mice served as the control group. Thirty 3-month-old male APP/PS1 mice were randomly allocated into a model group, a low-dose DSS(DSS-L, 3.2 g·kg~(-1)) group, a medium-dose DSS(DSS-M, 6.4 g·kg~(-1)) group, a high-dose DSS(DSS-H, 12.8 g·kg~(-1)) group, and a ketogenic diet(KD) group. The control and model groups received 8 weeks of normal saline gavage, while the DSS-L, DSS-M, and DSS-H groups received corresponding concentrations of DSS via gavage for 8 weeks. The KD group was fed the ketogenic diet for 8 weeks. After 8 weeks of treatment, the Morris water maze test, novel object recognition test, Y-maze test, and open field test were carried out to evaluate the cognitive function, memory processing, spatial memory, and spontaneous activity and exploratory behavior, respectively. A Roche meter was used to measure the fasting blood glucose level. The β-hydroxybutyrate(BHB) and lactate levels in the liver and brain tissue were quantified by the microplate assay. The adenosine triphosphate(ATP) and adenosine diphosphate(ADP) levels were detected by chemiluminescence. ELISA was employed to measure the serum level of insulin and brain tissue levels of mitochondrial complexes Ⅰ-Ⅳ, citrate synthase(CS), isocitrate dehydrogenase(ICD), and α-ketoglutarate dehydrogenase(α-KG). Immunofluorescence assay was employed to detect the expression of monocarboxylate transporter 2(MCT2) in the hippocampus. Western blot was used to determine the expression levels of 3-hydroxy-3-methylglutaryl-coenzyme A synthase 2(HMGCS2) in the liver, as well as 3-oxoglutarate-CoA transferase(OXCT1) and 3-hydroxybutyrate dehydrogenase(BDH1) in the brain. The results showed that compared with the control group, the model group exhibited reduced time and distance in the target quadrant in the Morris water maze, weakened novel object recognition, decreased Y-maze alternation percentage, and reduced distance and average speed in the open field(P<0.01, P<0.001). Furthermore, the model group exhibited raised levels of fasting blood glucose, insulin in the serum, and lactic acid in the brain, declined level of BHB in the liver(P<0.05, P<0.01), reduced levels of mitochondrial respiratory chain complexes Ⅰ-Ⅳ, CS, ICD, α-KG, ADP and ATP in the brain tissue(P<0.01, P<0.001), down-regulated expression of HMGCS2 in the liver, OXCT1 in the cortex and hippocampus, and BDH1 in the hippocampus(P<0.05, P<0.01). Compared with the model group, the DSS groups and the KD group showed increases in time in the target quadrant, levels of BHB in the liver and brain, mitochondrial complexes Ⅰ and Ⅳ, CS, α-KG, and ATP, and expression of BDH1 in the hippocampus and OXCT1 in the cortex, and reduced levels of fasting blood glucose, insulin in the serum, and lactate in the brain(P<0.05, P<0.01). All the DSS groups exhibited increased average speed in the open field test(P<0.05, P<0.01). The distance in the target quadrant, levels of mitochondrial complexes Ⅱ and Ⅲ, ICD, and ADP, and expression of BDH1 in the cortex increased in the DSS-M, DSS-H, and KD groups(P<0.05, P<0.01). The novel object recognition index and HMGCS2 expression in the liver raised in the DSS-L, DSS-H, and KD groups(P<0.05, P<0.01). The total distance traveled in the open field test increased in the DSS-L, DSS-M, and KD groups(P<0.05, P<0.01). The percentage of alternation in the Y-maze test and MCT2 expression level in the DG region increased in the KD group(P<0.05). In addition, the OXCT1 expression level in the hippocampus was up-regulated in the DSS-H and KD groups(P<0.05, P<0.01). DSS can promote the generation of ketone bodies in the liver and the transport and utilization of ketone bodies in the brain tissue, thereby alleviating the brain energy crisis and cognitive impairment of APP/PS1 mice.

Angelica sinensis (Oliv.) Diels (A. sinensis), commonly known as Danggui, is a chemically complex medicinal plant widely used in East Asian medicine and reported to exert anti-inflammatory, antioxidant, immunomodulatory, hematopoietic, neuroprotective, vasoprotective, metabolic, and tissue-repair effects. This narrative translational review evaluates literature published up to May 2026 and reappraises A. sinensis through a constituent-specific and exposure-relevant framework, focusing on phthalides, ferulic acid-related phenolic acids, polysaccharides, and representative preparations. Phthalides are mainly associated with neurovascular protection, mitochondrial homeostasis, autophagy/mitophagy regulation, and anti-apoptotic responses, but their translational relevance is constrained by chemical instability and low oral exposure. Ferulic acid and related phenolic acids are more consistently linked to inflammatory attenuation, redox regulation, epithelial barrier protection, and metabolic stress responses; however, many in vitro studies use concentrations exceeding plausible free systemic exposure. Polysaccharides are most strongly associated with hematopoietic support, immune modulation, gut microbiota regulation, metabolic homeostasis, and microenvironmental remodeling, although structural heterogeneity limits cross-study comparability. Direct clinical evidence for single-herb A. sinensis remains limited, and most clinical signals derive from multi-herb formulas. Overall, this review highlights the importance of distinguishing constituent-specific mechanisms, exposure plausibility, and attribution directness when evaluating the translational potential of A. sinensis.

This study investigated the protective effects of DBD against Staphylococcus aureus (S. aureus)-induced mastitis in mice and explored whether these effects were associated with gut microbiota alterations, blood-milk barrier integrity, and inflammatory signaling. A lactating mouse model of mastitis was established, and the effects of DBD were evaluated using HPLC, histopathological analysis, ELISA, qRT-PCR, Western blotting, immunofluorescence, and 16S rRNA sequencing. The results showed that DBD significantly reduced bacterial loads in mammary tissues, decreased the expression of pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6, and alleviated inflammatory cell infiltration and tissue damage. Moreover, DBD upregulated the expression of tight junction proteins and improved the integrity of the blood-milk barrier. DBD treatment was also associated with alterations in gut microbiota composition, as reflected by changes in the relative abundance of several bacterial taxa. In addition, DBD inhibited the activation of the NF-κB/NLRP3 and MAPK inflammatory signaling pathways. Collectively, these findings indicate that DBD alleviates S. aureus-induced mastitis accompanied by alterations in gut microbiota composition, suppressing inflammatory responses, and repairing the blood-milk barrier, suggesting its potential as a therapeutic agent for mastitis.

Systems biology research has integrated network pharmacology with clinical data to investigate traditional Chinese Medicine (TCM) antifibrotic mechanisms across multiple biological pathways. These combined approaches draw on chemical-protein interaction databases, transcriptomic and metabolomic profiling, protein-protein interaction networks, molecular docking, randomized trial and large cohort study evidence. Yinchenhao Decoction, Danggui Liuhuang Decoction, Curcumae Rhizoma (Ezhu in Chinese)-Astragali Radix (Huangqi in Chinese) herb pair, and Angelicae Sinensis Radix (Danggui in Chinese)-Chuanxiong Rhizoma (Chuanxiong in Chinese) herb pair regulate transforming growth factor-β (TGF-β)/mothers against decapentaplegic homolog (Smad), phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt), nuclear factor-κB (NF-κB), mitogen-activated protein kinase (MAPK), and janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathways. Integration of these signals is associated with suppression of inflammation, altered regulation of apoptosis, modulation of cellular activation, and extracellular matrix remodeling in hepatic, cardiac, and pulmonary fibrosis models. This multi-layered framework offers a rational basis for hypothesis generation in drug repositioning and development of novel antifibrotic candidates, although clinical validation remains limited and further rigorous trials are warranted.