This study aims to systematically retrieve and sort out the clinical research evidence of oral Chinese patent medicines in the treatment of vascular dementia (VaD) and understand the distribution and quality of the existing evidence in this field. PubMed, Web of Science, Cochrane Library, EMbase, CNKI, VIP, Wanfang, and SinoMed databases were retrieved from their establishment to November 5, 2024. Evidence diagrams were used to comprehensively present the data distribution characteristics. A total of 211 pieces of literature were included, among which 176 were RCTs, 11 were non-RCTs, 3 were retrospective studies, 1 was cohort study, 17 were systematic reviews/Meta-analyses, and 3 were expert recommendations or consensuses. It involves 45 kinds of Chinese patent medicines. Among them, Ginkgo Leave Tablets/Capsules are the most widely used. Most of the research periods are 8-12 weeks, and the sample size is 51-100 cases. The main outcome indicators include clinical efficacy, cognitive function evaluation, quality of life evaluation, safety indicators, neurological function indicators, hemorheological indicators, etc. The literature quality of RCTs, non-RCTs, and systematic reviews/Meta-analyses are generally not high, and the quality level of evidence is relatively low. Most studies have shown that oral Chinese patent medicines have potential efficacy in the treatment of VaD, but there is a lack of high-quality clinical evidence. Chinese patent medicines have advantages in the treatment of VaD, but there is still a lack of high-quality studies. This suggests that in future clinical research, large-sample and multi-center RCTs need to be carried out. Meanwhile, clinical research design and reporting should be standardized in accordance with relevant guidelines or tools to explore the characteristic advantages of oral Chinese patent medicines in the treatment of VaD, select reasonable outcome indicators, and strive to improve the quality of clinical research in TCM. This will help standardize the research plan, produce advanced evidence-based medical evidence with rigor and scientificity, and provide strong support for the prevention and treatment of VaD with TCM.

This study is aimed to investigate the therapeutic effects of Junren Bufei Yixin Granules (JRBF) on hypoxic pulmonary hypertension (HPH) and explore the therapeutic mechanism through the polypyrimidine tract-binding protein 1 (PTBP1)/pyruvate kinase isozyme type M2 (PKM2) signaling pathway. Sixty SPF-grade C57BL/6 male mice were randomized into normal, model, sildenafil, and low/medium/high-dose JRBF groups. HPH was induced by hypoxic exposure (10% O₂, 8 h/day) for 4 weeks. The right ventricular systolic pressure (RVSP) was measured by right cardiac catheterization. Echocardiography was employed record the pulmonary artery acceleration time (PAAT), pulmonary ejection time (PET), tricuspid annular plane systolic excursion (TAPSE), and right ventricular anterior wall thickness at diastole (RVAWd). The histopathological changes were observed by hematoxylin-eosin (HE) and Masson staining. Western blot was employed to measure the expression levels of PTBP1, PKM2, and PKM1 in the lung tissue. The immunofluorescence assay was employed to detect the co-localization of PTBP1 with the marker alpha-smooth muscle actin (α-SMA) of pulmonary arterial smooth muscle cells (PASMCs). The lactate assay kit was used to measure the lactate levels in the serum and lung tissue. In the cell experiments, the hypoxia model was established by exposing human pulmonary artery smooth muscle cells (hPASMCs) to 1% O₂ for 48 h. The optimal (10%) JRBF concentration for intervention was determined by the cell-counting kit-8 (CCK-8). The cell proliferation (EdU), migration (Transwell), PTBP1/PKM2/PKM1, and lactate production were analyzed. The results showed that JRBF significantly reduced the RVSP, improved the PAAT/PET ratio and TAPSE, and attenuated pulmonary arteriolar remodeling and myocardial fibrosis. Furthermore, JRBF suppressed PTBP1 and PKM2 expression and reduced the lactate accumulation in the lung tissue and PASMCs. The cell experiment results showed that the 10% JRBF-containing serum inhibited the proliferation and migration of hPASMCs, while decreasing the PTBP1/PKM2 expression and lactate production. In conclusion, JRBF mitigates HPH progression by suppressing the PTBP1/PKM2 axis and restoring the glycolytic flux.

Influenza viral pneumonia (IVP) is an infectious disease caused by influenza virus invading the lungs. With acute onset and rapid progression, it can lead to respiratory failure and even death in severe cases. Moreover, IVP is prone to cause large-scale incidence along with influenza epidemics, posing a serious threat to public health. The pathogenesis of IVP is complex, involving multiple pathological links such as viral replication, cytokine storm, immune imbalance, and oxidative stress. Studies have confirmed that the occurrence and development of IVP are closely related to signaling pathways including Toll-like receptors (TLRs)/nuclear factor-κB (NF-κB), Janus kinase (JAK)/signal transducer and activator of transcription (STAT), NOD-like receptor pyrin domain-containing protein 3 (NLRP3), mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase(PI3K)/protein kinase B (AKT), and nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1). TCM characterized by multi-pathway, multi-component, and multi-target actions shows unique potential in regulating the above pathways and ameliorating pathological damage in the lungs. Accordingly, this article clarifies the IVP pathogenesis mediated by these pathways and systematically reviews the recent research on TCM active ingredients, single herbs, and compound preparations in preventing and treating IVP via regulating these pathways, with focuses on the roles of TCM in inhibiting viral replication, regulating inflammation, restoring immune homeostasis, and alleviating oxidative stress damage. It aims to comprehensively reveal the potential mechanisms of TCM in treating IVP, providing new insights for clinical diagnosis and treatment of IVP.

This study aimed to investigate the mechanisms by which Acanthopanax senticosus extract (ASH) exerts effects onα-synuclein (α-syn) overexpressing transgenic mouse model of Parkinson's disease (PD), with a focus on its regulation of brain lipid metabolism. Twenty PD model mice were randomly assigned to a model group or an ASH treatment group (45.5 mg·kg^-1 by gavage for 4 weeks), and 10 C57BL/6 mice served as a normal control group. Behavioral assessments revealed that, compared with controls, PD model mice showed prolonged pole test time, reduced spontaneous locomotor activity, shorter latency to fall in the rotarod test, and decreased total distance traveled in the open field test. Serum levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), caspase-9 were significantly elevated, B-cell lymphoma-2 (Bcl-2), and proliferating cell nuclear antigen (PCNA) expression was reduced, and marked neuronal damage was observed in brain tissue. ASH intervention significantly improved these behavioral and biochemical parameters and attenuated neuronal injury. Untargeted lipidomics analysis revealed significant alterations in sphingomyelin (SM), ceramide (Cer), phosphatidylcholine (PC), and phosphatidylserine (PS) across multiple brain regions (cortex, substantia nigra, cerebellum, and striatum) in PD mice, which were notably restored by ASH treatment. Pathway analysis indicated that these metabolites were predominantly involved in sphingolipid metabolism. Western blot further demonstrated that ASH downregulated the expression of key sphingolipid metabolic enzymes serine palmitoyltransferase long-chain base subunits 1 and 2 (SPTLC1 and SPTLC2) and upregulated UDP-glucose ceramide glucosyltransferase (UGCG), β-galactosylceramidase (GALC), and sphingosine kinase 2 (SPHK2), thereby suppressing abnormal SM and Cer accumulation in the substantia nigra and elevating PS and PC levels in the striatum. Spearman's correlation analysis supported the modulatory effect of ASH on brain lipid metabolic profiles. In conclusion, ASH improves behavioral deficits, exerts anti-inflammatory effects, and regulates sphingolipid metabolism to correct disordered lipid profiles, thereby providing neuroprotective effects in PD mice.

Based on the holistic regulation and multi-target characteristics of TCM, this study investigated the mechanism of Panlongqi Tablets (PLQT) in ameliorating rheumatoid arthritis (RA) by regulating key proteins, including glycogen synthase kinase-3β (GSK-3β), phosphatidylinositol 3-kinase catalytic subunit alpha (PIK3CA), and protein kinase B3 (AKT3), within the PI3K-AKT signaling pathway. An adjuvant-induced arthritis (AIA) rat model was established by intradermal injection of type Ⅱ collagen-Freund's complete adjuvant into the right hind paw, and rats received different doses of PLQT for intervention. Pharmacodynamic effects were evaluated by monitoring changes in body weight, measuring paw swelling, observing ankle synovial tissue pathology via hematoxylin-eosin (HE) staining, and detecting serum levels of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β), using ELISA. Targets identified through prior network pharmacology screening were integrated with therapy-related biomarkers from untargeted metabolomics for key pathway enrichment and identification of critical targets. Western blot and RT-qPCR were subsequently used to validate the expression of these key targets. Animal experimental results showed that, compared with the model group, all PLQT dose groups significantly improved weight loss, reduced paw swelling, inhibited synovial tissue fibrosis hyperplasia and inflammatory cell infiltration, and decreased serum levels of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β in RA rats, exhibiting a partial dose-dependent manner. Metabolomics analysis revealed that PLQT exerted regulatory effects on 179 of 276 RA-related biomarkers. Enrichment analysis revealed that GSK-3β, PIK3CA, and AKT3 proteins in the PI3K-AKT signaling pathway were the key targets for PLQT intervention in RA. Validation by Western blot and RT-qPCR demonstrated that PLQT significantly modulated the expression of these three proteins. In conclusion, the therapeutic effects of PLQT on RA are likely associated with regulation of GSK-3β, PIK3CA, and AKT3 within the PI3K-AKT signaling pathway.

To analyze the changing pattern of blood stasis degree in different TCM syndromes of non-traumatic osteonecrosis of femoral head (NONFH), the present study adopted a retrospective cross-sectional design. The clinical and digital subtraction angiography (DSA) data were collected from 60 NONFH patients with blood stasis syndrome treated at the Third Affiliated Hospital of Beijing University of Chinese Medicine from February 2022 to March 2025. According to Chinese Medicine Identification Criteria for Necrosis of the Femoral Head (2019 edition), 60 patients were allocated into three groups of phlegm-stasis obstruction of collaterals, meridian obstruction, and liver-kidney deficiency, with 20 patients in each group. The morphological features of blood vessels were observed by DSA, and the diameter of the profunda femoris artery, diameters of medial/lateral circumflex femoral arteries, and vessel count were recorded. The degrees of blood stasis in different syndrome groups were analyzed. The results showed that there were 38 males and 22 females among the 60 patients, with mean age of (41.18±14.56) years. Two, thirty-three, twenty-two, and one patients were in ARCO stages Ⅰ, Ⅱ, Ⅲ and Ⅳ, respectively. There was no difference in the baseline data (age, BMI, etc.) among the three groups. Regarding the vascular parameters, the meridian obstruction group had the profunda femoris artery diameter of (6.59±0.94) mm, medial circumflex femoral artery diameter of (2.99±0.42) mm, medial/lateral ratio of 0.50 (0.43, 0.58), and total number of arteries being 8.00 (7.00, 8.00), which were all lower than those in the phlegm-stasis obstruction group and the liver-kidney deficiency group (P<0.05, P<0.01). The results indicated that the DSA of NONFH patients with blood stasis presented abnormal vascular morphology, and their vascular images showed a certain pattern throughout the disease course, with lower vessel diameter and count in the middle stage. This result suggested that the degree of blood stasis in the patients varied from mild to severe and back again with the progression of the disease. This study not only provides quantifiable imaging indicators for the macroscopic diagnosis of blood stasis syndrome and verify its dynamic evolution law, but also suggests that in clinical practice, imaging techniques such as DSA can be used to assist in syndrome differentiation and classification. This provides objective references for staged treatment and the optimization of intervention timing and intensity of blood-activating and stasis-resolving regimens.

This study aims to investigate the clinical efficacy and underlying mechanism of Huoxue Tongbi Formula in treating patients with steroid-induced osteonecrosis of the femoral head (SONFH) with meridian blockage syndrome. A total of 40 patients with SONFH and meridian blockage syndrome were retrospectively enrolled. Demographic data, clinical efficacy scores (pain and hip joint function), Harris scores, hip joint range of motion, imaging indices (ARCO stage, BUCMXE, bone marrow edema, and joint effusion), symptom/syndrome scores, and coagulation-related physiochemical indices (complete blood count, four coagulation tests, and four thrombosis tests) were collected and compared before treatment and after three months of treatment. Peripheral blood samples from three patients with significant efficacy were subjected to transcriptome sequencing before and after treatment to screen differentially expressed genes (DEGs). GO and KEGG enrichment and PPI network analysis were performed. Genes most relevant to the core phenotype of SONFH with meridian blockage syndrome were identified using Spearman correlation analysis. The results showed that Huoxue Tongbi Formula significantly improved the clinical efficacy scores (including pain and hip joint flexion function), Harris scores, and range of internal and external rotation of the hip (P<0.01). It also maintained stable imaging indices, alleviated various blood stasis-related clinical symptoms (hip pain, fixed pain, lower limb weakness) (P<0.05, P<0.001), and significantly reduced thrombin-antithrombin complex (TAT) levels (P< 0.01). Transcriptome analysis identified 368 DEGs (274 upregulated and 94 downregulated). GO functional enrichment revealed that the biological processes involved by DEGs mainly include positive regulation of tumor necrosis factor production, integrin-mediated signaling pathways, neutrophil chemotaxis, and regulation of tumor necrosis factor production. KEGG enrichment analysis revealed that these DEGs were primarily involved in pathways such as hematopoietic cell lineage, osteoclast differentiation, complement and coagulation cascades, and platelet activation. PPI network analysis combined with correlation analysis identified core genes UBA52 (r=0.83, P<0.05), RACK1 (r=0.88, P<0.05), and RPL19 (r=-0.87, P<0.05) were significantly correlated with blood stasis syndrome scores. CD74 was significantly correlated with osteonecrotic lesions (r=0.95, P<0.05) and TAT (r=0.88, P<0.05). These findings indicate that Huoxue Tongbi Formula ameliorates clinical symptoms and certain imaging indices in SONFH patients with meridian blockage syndrome by regulating hematopoiesis and bone metabolism (inhibiting osteoclast activity) and correcting hypercoagulability (inhibiting coagulation activation). Core genes such as UBA52, RACK1, and RPS3A may be key molecules linking blood stasis syndrome to the regulation of the coagulation-bone metabolism network.

This study aimed to elucidate the mechanisms of diosgenin, a natural compound derived from traditional Chinese medicine, on the triple-negative breast cancer cell line MDA-MB-231, with a focus on its induction of cell cycle arrest and inhibition of cell migration. Multiple experimental approaches were employed, including RNA sequencing analysis, flow cytometry for cell cycle detection, wound healing assays to evaluate migration capacity, F-actin staining to observe cytoskeletal changes, transmission electron microscopy (TEM) to examine cellular morphology and filopodia alterations, as well as Western blot and immunofluorescence staining to detect the expression of related proteins. RNA sequencing revealed significant gene expression differences between the diosgenin-treated group and the control group, with KEGG and GO analyses showing enrichment of differentially expressed genes mainly in pathways related to cell cycle and migration. Flow cytometry demonstrated that diosgenin induced G₀/G₁ phase arrest in MDA-MB-231 cells in a dose-dependent manner. Further Western blot and immunofluorescence assays indicated that diosgenin regulated the cell cycle via the CDC25A-CDK2/4/6 axis. Wound healing assays showed that diosgenin significantly inhibited cell migration. F-actin staining indicated that diosgenin suppressed F-actin formation and disrupted its structure. TEM observations revealed a reduction in filopodia formation on the cell surface after diosgenin treatment. Moreover, Western blot and immunofluorescence results demonstrated that diosgenin inhibited migration by suppressing epithelial-mesenchymal transition (EMT) and the RhoA-ROCK1 signaling pathway. In conclusion, diosgenin induces G₀/G₁ phase arrest in MDA-MB-231 cells by regulating cell cycle-related proteins and significantly inhibits cell migration by suppressing F-actin formation, reducing filopodia on the cell surface, and inhibiting EMT and the RhoA-ROCK1 pathway.

Non-alcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease worldwide, characterized primarily by hepatic inflammation and dysregulated lipid metabolism. As a classic representative formula of the "bitter-purging method", Modified Wushi Xiexin Decoction has demonstrated definite clinical efficacy; however, its anti-inflammatory effects and underlying mechanisms in the treatment of NAFLD remain unclear. This study combines network pharmacology with animal experimental validation to evaluate the therapeutic effect of Modified Wushi Xiexin Decoction on NAFLD and reveal its potential mechanisms of action. Drug targets were collected from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP). NAFLD-related disease targets were retrieved from the Therapeutic Target Database (TTD), GeneCards, Online Mendelian Inheritance in Man (OMIM), Pharmacogenomics Knowledge Base (PharmGKB), and Comparative Toxicogenomics Database (CTD). R software was used to screen the intersection targets of the two sets. Core target analysis and network visualization were performed by using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database and Cytoscape 3.8.2 software. R software was applied for Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Core targets were analyzed based on the Gene Expression Omnibus (GEO) database, and receiver operating characteristic (ROC) curves were plotted to evaluate the diagnostic efficacy of the core targets. For animal experimental validation, a NAFLD mouse model was established by feeding a 60% high-fat diet combined with intraperitoneal injection of streptozotocin. Pathological improvements were assessed by hematoxylin-eosin (HE) staining and oil red O staining. Enzyme-linked immunosorbent assay (ELISA) was used to detect the level of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) in liver tissue. Immunohistochemistry (IHC) and Western blot (WB) were performed to measure the expression of Toll-like receptor 4 (TLR4), nuclear factor-κB (NF-κB), and NOD-like receptor protein 3 (NLRP3) proteins in mouse liver tissue. Network pharmacology identified 97 active components, 108 intersection targets, and 10 core targets of Modified Wushi Xiexin Decoction. GO enrichment analysis indicated that anti-NAFLD effects were exerted by regulating biological processes such as oxidative stress and nutritional levels. KEGG enrichment analysis mainly involved signaling pathways, including TLR, NF-κB, and TNF. The GEO database indicates that there is a significant difference in TLR4 expression between healthy individuals and NAFLD patients (P<0.05), with the area under the ROC curve (AUC) being greater than 0.810, suggesting a high diagnostic efficacy. Animal experiments showed that Modified Wushi Xiexin Decoction could alleviate pathological damage in the liver tissue of NAFLD mice, reduce blood lipids, improve liver function, and downregulate the expression of inflammatory factors in liver tissue. IHC and WB confirmed that Modified Wushi Xiexin Decoction could downregulate the TLR4 expression, inhibit NF-κB activity, and suppress NLRP3 inflammasome activation. In conclusion, Modified Wushi Xiexin Decoction may alleviate inflammatory responses and improve liver function and blood lipids in NAFLD by regulating the TLR4/NF-κB signaling pathway and inhibiting NLRP3 inflammasome activation, thereby exerting therapeutic effects on NAFLD.

Poria cocos is a commonly used bulk traditional Chinese medicinal material, with multiple parts used medicinally, such as Poriae Cutis, Rubra Poria, White Poria, and Poria cum Radix Pini. Polysaccharides are their main active components. Clarifying the composition and content differences of polysaccharides in different medicinal parts of P. cocos can provide a reference for processing and clinical application of P. cocos medicinal materials and decoction pieces. In this paper, high-performance gel permeation chromatography (HPGPC) and nuclear magnetic resonance (NMR) spectroscopy were employed to qualitatively compare the relative molecular mass distribution and chemical composition of alkali-soluble polysaccharides from different parts of crude P. cocos. The results showed that the composition of alkali-soluble polysaccharides in Rubra Poria and Poriae Cutis was consistent with that in White Poria, all of which were β-(1→3) -D-glucans. The relative molecular mass distribution was also relatively close, ranging approximately from 9.13×10⁴ to 1.04×10⁵. On the basis of the content determination method of β-(1→3) -D-glucan in P. cocos according to the 2025 edition of Chinese Pharmacopoeia, the preparation method of the test sample solution was optimized. Firstly, a desalination step was added, which can enable the test sample chromatogram to present only the chromatographic peak of glucose, thereby reducing the difficulty of separation. Secondly, this experiment discovered for the first time that under acidic conditions, the hydrolysis of β-(1→3) -D-glucan to glucose was accompanied by the generation of a small amount of 5-hydroxymethylfurfural (5-HMF) as a by-product. A more intense acid hydrolysis reaction condition indicated a greater conversion yield of 5-HMF. Therefore, according to the results of single-factor experiments and response surface methodology experiments, the acid hydrolysis time was shortened from 6 h to 1.5 h, which improved the analysis efficiency. After verification, the optimized method was simple and stable, and had good repeatability and accuracy. Then, the optimized quantitative method was used to evaluate the content of β-(1→3) -D-glucan in different parts of crude P. cocos and decoction pieces. The results demonstrated that the content of β-(1→3) -D-glucan in different medicinal parts of P. cocos was in the order of White Poria, Poria cum Radix Pini, Rubra Poria, and Poriae Cutis. Among the commercially available Poria decoction pieces, the content of β-(1→3) -D-glucan in the white and hard decoction pieces was higher than that in the dark and loose-textured decoction pieces.