To explore the medication rule and pharmacological activity of the core combination of chrysanthemi flos,the drug frequency, complex network and association rules of Chrysanthemum prescriptions were analyzed. The network pharmacology research method was used to construct the "herbs-key target-disease" of core combination drugs. Combined with the forecast results, an in vitro cell model was used to evaluate the pharmacological effects of chrysanthemi flos drug combinations. A total of 92 prescriptions containing chrysanthemi flos were obtained, involving 212 herbs, and 32 herbs with frequency greater than or equal to 10.The association rules showed that the sustain and confidence degree of chrysanthemi flos-Glycyrrhizae radix et rhizoma were the highest, and chrysanthemi flos-glycyrrhizae radix et rhizoma-schizonepetae herba, chrysanthemi flos-glycyrrhizae radix et rhizoma-schizonepetae herba-chuanxiong rhizoma, chrysanthemi flos-glycyrrhizae radix et rhizome-schizonepetae herba-chuanxiong rhizome-saposhnikoviae radix were next to each other, respectively. Network pharmacology analysis showed that the core drug combination of chrysanthemi flos-glycyrrhizae radix et rhizoma could treat tumors, digestive system diseases, nervous system diseases and other diseases. In vitro cell activity study showed that the combination of chrysanthemi flos and glycyrrhizae radix et rhizoma had a better inhibition rate on NO levels than the single drug. Compared with the single use of chrysanthemi flos, the combination of drugs showed more significantactivity, reflecting the scientificity of compatibility of TCM in clinic.

The pharmacological method of traditional Chinese medicine serum was used to explore the effect of Banxiaxiexin Decoction (BXD) on the proliferation of different gastric cancer cells in vitro. Additionally,the preparation conditions of BXD drug-containing serums were examined toobserve the pharmacodynamics of gastric cancer cells. Blood was collected at intervals of 30, 60, 90, 120, and 150 minutes after high, medium, and low intragastric gavage of BXD to prepare drug-containing serums. Based on the selected gavage doses and blood collection times, MGC803, MKN45, AGS, and HGC27 cells were exposed to 5%~50% concentrations of drug-containing serum, and CCK8 assay was employed to detect the inhibitory effects of different gavage doses, blood collection times, and volume fractions of BXD drug-containing serum on the proliferation of gastric cancer cells. The test results showed that compared with other time points, all BXD drug-containing serums had the strongest inhibitory effect on gastric cancer cells at the blood collection time of 120 minutes. Compared with the low-dose BXD group, the medium-dose BXD group had a strong inhibitory effect on gastric cancer cells, and there was no significant difference between the medium-dose and high-dose BXD groups. Based on the analysis of the inhibitory effects of 10 concentrations ranging from 5% to 50% on different gastric cancer cells, the IC₅₀ values of all drug-containing serums collected 120 minutes after gavage in the medium-dose BXD group were 20%. Analysis of the inhibitory effects of different gavage doses, blood collection times, and volume fractions on different gastric cancer cells revealed that a medium dose of BXD, blood collection time of 120 minutes,and a volume fraction of 20% had the strongest inhibitory effect on gastric cancer cells. Therefore, the medicated serum with a blood collection time of 120 minutes and a volume fraction of 20% in the medium-dose BXD group had the best pharmacodynamic effect on gastric cancer cells.

Based on bioinformatics, this study validates the mechanism of action of Haitongpi-Tougucao (compound Haitongpi) in inhibiting lipopolysaccharide (LPS)-induced ferroptosis in rat inflammatory chondrocytes. Bioinformatics tools were used to predict the mechanism of action of ferroptosis in osteoarthritis and identify pathways for validation. The key techniques used were as follows: the detection of ferrous ion content and reduced glutathione (GSH) content using relevant kits; the detection of cell viability and the levels of related cytokines IL-1β, IL-6, and TNF-α using the enzyme-linked immunosorbent assay (ELISA) after dosing; and the use of protein immunoblotting (western blot, WB) to detect the protein expression levels of NLRP3, Caspase-1, ASC, and GPX4, a gene that inhibits ferroptosis, related to the NLRP3 inflammasome pathway in each group. The results revealed that the ferrous ion content was significantly decreased,while the GSH content was significantly increased; the ELISA experiment showed that the levels of inflammatory factors IL-1β, IL-6, and TNF-α were decreased in each group administered with the drug compared with those in the model group; the WB results showed that the expression levels of NLRP3, Caspase-1, and ASC proteins were significantly decreased and GPX4 protein expression levels were significantly increased in each group administered with a specific dosage of the drug compared with those in the model group. Therefore, the compound Haitongpi can intervene in the ferroptosis of inflammatory chondrocytes by mediating the NLRP3 inflammasome pathway, thereby achieving the purpose of osteoarthritis treatment.

Based on network pharmacology, molecular docking, and in vitro experiments, this study explores the molecular mechanism of quercetin against colorectal cancer through the p53 signaling pathway. The drug targets quercetin, and the disease targets colorectal cancer, which was obtained via the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform and Gene Cards database, respectively. The common drug and disease targets were mapped using a Venn diagram, and the protein-protein interaction network map was constructed with the help of the String database and Cytoscape_v3.7.2 software. At the same time, GO and KEGG enrichment analysis, molecular docking, core target expression, and survival analysis were also performed. Finally, cell proliferation activity, level of apoptosis, cell cycle arrest, and changes in the expression of core targets and key proteins of the p53 pathway were detected through cellular experiments. Network pharmacology suggests that AKT1 and TP53 are the core targets of quercetin against colorectal cancer, GO and KEGG analysis demonstrate that quercetin is mainly involved in the PI3K/Akt and p53 signaling pathways, molecular docking demonstrates that quercetin exhibits strong binding activity with the core targets AKT1 and TP53, and TP53 is found to be both highly expressed in colorectal cancerand also affect the survival and prognosis of patients with colorectal cancer. The results of cellular experiments show that quercetin can inhibit the proliferation of HCT-116 cells, induce G₀/G₁ cell-cycle arrest in HCT-116 cells, and promote apoptosis. This mechanism may regulate core targets such as TP53 and AKT1, activate the p53 signaling pathway, participate in the proliferation and apoptosis of HCT-116 cells, and thus function to resist colorectal cancer.

The aim of this study was to explore the potential effective ingredients and mechanism of action of Panax quinquefolius L. in anti-aging based on network pharmacology and molecular docking. The anti-aging activity of P. quinquefolius L. was evaluated in a zebrafish aging model. The active ingredients of P. quinquefolius L. and their potential targets related to anti-aging were screened using databases, and protein-protein interaction networks (PPI) were mapped to screen core targets. Enrichment analysis and molecular docking verification of the core targets were performed. SA-β-Gal staining results showed that P. quinquefolius L. exerted significant anti-aging activity.Database screening identified 11 active ingredients and 53 potential core targets of P. quinquefolius L. in anti-aging, such as AKT1, STAT3, and JUN. The results of GO and KEGG analysis showed that the anti-aging effects of P. quinquefolius L. may involve factors including xenobiotic stimulus response, negative regulation of apoptotic processes, PI3K-AKT signaling pathway, ErbB signaling pathway. Molecular docking results showed that polyacetylene PQ-2 and PQ-2 were tightly bound with their core targets, and tight binding was also seen with AKT1 and HRAS with various active ingredients. P. quinquefolius L. may act on multiple targets such as AKT1, HRAS, and MAPK1 through polyacetylene PQ-2, PQ-2, and other ingredients, and then regulate multiple pathways such as endocrine resistance, ErbB signaling pathway, and other mechanisms to exert an anti-aging effect.Collectively, these dataprovide a theoretical basis for the application of P. quinquefolius L. in anti-aging.

This study aimed to investigate the antifatigue effects and mechanisms of Dioscorea opposita Thunb. polysaccharides (DTPs) on exercise-related fatigue in mice. In a mouse model of exercise fatigue where mice were subjected to exhaustive swimming and fatigue rotarod, changes in exhaustive swimming duration, body weight, fatigue metabolite accumulation, activity levels of related enzymes, liver tissue structure, and muscle glycogen (MuG) and liver glycogen (LG) contents were assessed. The results demonstrated that DTPs significantly prolonged the exhaustive swimming duration and reduced body weight loss, hepatic damage, and serum lactic acid (LD), blood urea nitrogen (BUN), and lactate dehydrogenase (LDH) levels in the mice. DTPs also significantly enhanced superoxide dismutase (SOD) activity and MuG and LG contents and significantly reduced aspartate aminotransferase (AST) levels. Additionally, in mice administered DTPs, the mRNA expression of phosphoinositide 3-kinase (PI3K) was significantly upregulated, whereas that of protein kinase B (AKT) and glycogen synthase kinase-3 (Gsk-3β) was significantly downregulated in skeletal muscle. Taken together, DTPs can reduce metabolite accumulation and ameliorate exercise fatigue by regulating the PI3K/AKT/Gsk-3β pathway to promote glycogen synthesis.

The aim of this study is to investigate the mechanism action of indole acetylated high-amylose maize starch in improving ulcerative colitis. Dextran sulfate sodium salt was used to induce acute ulcerative colitis in mice. Indole acetylated high-amylose maize starch was then used to target the colon with the delivery of indole-3-acetic acid. This was combined with the administration of an aryl hydrocarbon receptor inhibitor to analyze the mice in terms of colon length; disease activity index; and levels of interleukin-6, interleukin-10, transforming growth factor β1, myeloperoxidase, and interleukin-22 in the colon, which were detected by enzyme-linked immunosorbent assay. Quantitative polymerase chain reaction was used to analyze the relative expression levels of the colonic tight junction proteins occludin, ZO-1, and CYP1A1. Flow cytometry was used to test the ratio of regulatory T cells and T helper 17 cells in the mesenteric lymph nodes. The results showed that administration of indole acetylated high-amylose maize starch significantly alleviated the shortening of the colon length; significantly reduced the disease activity index and the levels of interleukin-6 and myeloperoxidase; significantly promoted the expression of interleukin-10, transforming growth factor β1, interleukin-22, CYP1A1, occludin, and ZO-1; significantly increased the proportion of regulatory T cells; and significantly reduced the proportion of T helper 17 cells. Administration of the aryl hydrocarbon receptor inhibitor weakened the effect of indole acetylated high-amylose maize starch. These results together suggest that acetylated high-amylose maize starch can improve ulcerative colitis by activating aryl hydrocarbon receptors.

Using light chromatography-mass spectrometry (LC-MS), network pharmacology, and animal experiments, we explored the molecular mechanism by which Xinjia Cistanche Tusi Decoction (XJCRTST) promotes follicular development through granulosa cell mitophagy. LC-MS and network pharmacology were used to screen for the main components of XJCRTST and its therapeutic targets and pathways related to hypoovarianism. Female Sprague-Dawley rats were divided into five groups: model group, western medicine group, and XJCRTST high dose, medium dose, and low dose groups. The morphological changes of the ovary were observed through hematoxylin and eosin staining, and the structure and morphology of mitochondria and mitophagosomes in ovarian granulosa cells were observed through transmission electron microscopy. Two hundred and fifty-two compounds were identified in XJCRTST, with 42 potential targets for treating hypoovarianism, and the Gene Ontology enrichment mainly involved biological process (1 168 items), cell composition(45 items), and molecular function(59 items). KEGG pathway enrichment showed that the pathways involved were AGE-RAGE, Prolactin and TNF signaling pathways. Three target genes Parkin/PINK1, HIF1A and MAPK8 were enriched in the Mitophagy-animal process.Animal experiments showed that the number of follicles increased and the atretic follicles decreased in the Chinese medicine treatment group. Electron microscopy found that mitochondrial swelling and mitophagy decreased in the Chinese medicine group. XJCRTST may play a therapeutic role in treating hypoovarianism by regulating mitochondrial function and mitophagy-related pathways in ovarian granulosa cells.

The aim of this study is to reveal the mechanism of Xuefuzhuyu oral liquid in treating thrombotic diseases and to explore its effective antithrombotic active ingredients. The Traditional Chinese Medicine Systems Pharmacology database was used to search for the active ingredients or related components of Xuefuzhuyu oral liquid. A protein-protein interaction network was constructed using the STRING database to obtain the core targets. A “component-target”network diagram was constructured using Cytoscape, which was used to perform topological,GO and KEGG enrichment analyses on core components to predict the antithrombotic mechanism action. Molecular docking was conducted on the key components and action targets according to the degree ranking. 81 core components, such as tumor necrosis factor (TNF), ALB, and AKT1 were obtained via network topology analysis screening.A total of 304 biological processes (BPs), 72 molecular functions, and 41 cell components were analyzed using GO enrichment analysis, and pathway enrichment yielded 80 signaling pathways, such as the coagulation cascade responseand TNF pathway.Molecular docking results showed that Sainfuran, Xambioona, and 7-methoxy-2-methyl isoflavone have good affinity with target proteins ESR1, F2, IL-2, KDR, MET, and MMP3. This study provides a reference for the application of Xuefuzhuyu oral liquid in antithrombotic therapies.

This study investigates the effects of Gandouling (GDL) tablets on ferroptosis in hepatolenticular degeneration in TX mice and their mechanism of action on the ferroptosis of HT22 cells induced by CuCl₂, based on the PKCβII/ACSL4/ ALOX5 signaling pathway. TX mice were divided into five groups: control, model, GDL tablet, Fer-1, and Glutathione. HT22 cells were also divided into five groups: control, model, GDL tablet, Fer-1, and GDL tablet + Fer-1. Hematoxylin and eosin staining was used to detect the pathological changes in the hippocampus tissues of the mice. Western blotting was used to detect the expression of PKCβⅡ, ACSL4, and ALOX5 in the hippocampus tissues and HT22 cells of the mice, as well as the expression of SLC7A11 and GPX4 in HT22 cells. The content of Fe²⁺ in the hippocampus tissues of the mice was detected via microassay. The levels of SOD, MDA, and GSH-Px in HT22 cells were detected by microplate assay. Finally, the expression of PKCβⅡ, ACSL4, and ALOX5 mRNA in HT22 cells was detected by quantitative real-time polymerase chain reaction. Compared with the control group, the hippocampus tissues of mice in the model group showed clear damage; the protein expression of PKCβⅡ, ACSL4, and ALOX5 showed a clear increase; the protein expression of SLC7A11 and GPX4 decreased significantly; and Fe²⁺content increased significantly (P<0.05). Compared with the model group, the pathological damage to hippocampus tissues showed improvements in the GDL tablet, Fer-1, and Glutathione group with the effects being noticeable in the GDL tablet group. It was possible to inhibit ferroptosis of HT22 cells in the GDL tablet and Fer-1 group and significantly lower their expression of PKCβⅡ, ACSL4, and ALOX5 protein and mRNA in comparison to the model group(P<0.05). The MDA contentalso decreased significantly (P<0.05) while the SOD activity and the GSH-Px content increased significantly(P<0.05). Thus, GDL tablets can inhibit ferroptosis in hippocampus tissues of TX mice andinhibit ferroptosis induced by CuCl₂ in HT22 cells. Moreover, the ferroptosis mechanism may be related to the down-regulation of the PKCβⅡ, ACSL4, and ALOX5 signaling pathway and the attenuation of intracellular lipid peroxidation.

We used the Gene Expression Omnibus database to identify targets associated with chronic obstructive pulmonary disease (COPD) and heart failure(HF). Then, we explored the chemical composition and targets of Fritillaria thunbergii-Trichosanthis fructus to determine their potential to regulate COPD complicated by HF. We analyzed the target function and pathway annotation to create a network of tissue-specific protein-protein interactions (PPI).A total of 227 targets were involved in regulating COPD complicated by HF progression through Fritillaria thunbergii-Trichosanthis fructus, including 153 upregulated and 74 downregulated genes.Topological analysis showed that the average median of the PPI network was 0.4, and the average degree value was 1.83, with key targets including RPS23, SNU13, NOL6, ELAVL1. The cellular components were mainly located in the endomembrane system, nuclear endosomes, and extracellular vesicles. Biological processes mainly involved vesicle-mediated transport, microtubule-based motility, and intracellular protein transport.The relevant signaling pathway was the MAPK signaling pathway.MCODE analysis revealed two core clusters: Cluster 1 involves genes such as TKT,ENO1, NCL, and KIF1B, which are involved in regulating the Golgi transport of kinesin and estrogen, and Cluster 2 involves genes such as SIN3B, PHF20, CTBP1, and XPNPEP1, which are involved in the regulation of histone-associated responses.Tissue-specific PPI networks in the auricles, left ventricle, and lungs suggest that the Fritillaria thunbergii-Trichosanthis fructus pairing may affect the progression of COPD complicated by HF through the regulation of the ELAVL1-ENO1-NCL axis.Molecular docking showed that the binding of trichosanic acid, the main active ingredient involved in relieving the chest and dispersing mass, and peimisine, the main ingredient involved in dissipating phlegm and dispersing mass, to the protein targets ELAVL1, ENO1, and NCL was highly stable, and that the binding of peimisine to said three target proteins was stronger than that of trichosanic acid.This indicates that the combination of the two ingredients is first used to treat the lungs and then to regulate the heart, and that they are mutually necessary, resulting in therapeutic effects on both the heart and lungs.

In this study, egg yolk lecithin, cholesterol,and ceramide were used as film-forming materials to prepare collagen ceramide liposomes (CO-CS) by the thin film dispersion method. To optimize the process, encapsulation efficiency was used as the response value, and it was evaluated by influencing factors such as drug-lipid ratio, film-material ratio, ultrasonic time, and hydration time. Results showed that encapsulation efficiency reached 90.73% when the drug-lipid ratio, film-material ratio, and ultrasonic time were 1:16, 4.3:1, and 8.5 min, respectively. Under these conditions, the particle size, polymer dispersity index (PDI), and zeta potential of CO-CS were(206.63±2.06) nm, 0.187±0.010, and (34.90±0.82) mV, respectively. After 60 days of storage at room temperature in the dark, the encapsulation efficiency was 87.2 %. Furthermore, the particle size, PDI, and zeta potential of CO-CS changed to (223.70±1.85) nm, 0.174±0.013, and (33.51±2.10) mV, respectively. In summary, CO-CS produced in this study revealed high encapsulation efficiency and good stability, and the preparation process is reasonable and feasible.

This study aimed to explore the material basis and mechanism of action of Monopterus albus peptides against hyperlipidemia using hyperlipidemic zebrafish model and network pharmacology. Analysis of the ameliorating effects of Monopterus albus peptides on hyperlipidemia was conducted by constructing a hyperlipidemic zebrafish model and measuring the dye staining signal intensity of triglyceride and cholesterol fluorescence intensity changes. Monopterus albus peptides and disease targets were filtered using BIOPEP-UWM, SwissTargetPrediction, GeneCards, STRING, and other databases. Target GO functional enrichment analysis and KEGG pathway enrichment analysis were performed using the DAVID bioinformatics software, and the Monopterus albus peptides-potential target-signaling pathway network and theprotein-protein interaction (PPI) network were constructed. The results showed that Monopterus albus peptides at mass concentrations of 62.5 μg/mL and 125.0 μg/mL significantly reduced the intensity of the triglyceride staining signal (p<0.01) and cholesterol fluorescence intensity (p<0.001) in the vasculature of hyperlipidemic zebrafish. The results of network pharmacology showed that there were 35 potentially active peptide sequences in Monopterus albus peptides, and 21 core targets were obtained by protein interaction analysis. GO and KEGG enrichment analyses indicated that Monopterus albus peptides were mainly involved in biological processes such asregulation of lipid metabolic processes, and exertan antihyperlipidemia effect viainflammation regulation, insulin resistance, and lipid and atherosclerosis channels. Initially, this study confirmed that Monopterus albus peptides have an antihyperlipidemia effect, and revealed that Monopterus albus peptides have multiple active peptide fragments, multiple targets, and multiple channels in the biological process of reducing blood lipid levels, which will provide a theoretical basis and reference for further in-depth research on the material basis of Monopterus albus peptides and their role and application in countering hyperlipidemia.

Based on the gene expression omnibus(GEO) database, combined with network pharmacology and molecular docking technology, we aimed to conduct reverse network pharmacology research from a molecular level to identify Chinese medicine with anti-hepatocellular carcinoma (HCC) activity. Relevant targets of HCC were acquired from databases including GEO, GeneCards, Online Mendelian Inheritance in Man, and Therapeutic Target Database. The core targets were identified using the String platform, and the core constituents were screened from the TCMIP(integrative pharmacology-based research platform of traditonal Chinese medicine) and TCMID(traditional Chinese medicine integraive database) databases. The core traditional Chinese medicine (TCM) was ultimately selected through the traditional Chinese medicine systems pharmacology database and analysis platform(TCMSP). Molecular docking technology and cellular experiments were employed to identify relevant screening results. A total of 398 important targets for HCC were found from the disease target databases, from which 8 core targets, 11 core constituents, and 1 core TCM (Puerariae Lobatae Radix) were further screened. Molecular docking results showed that three core constituents (quercetin, genistein, and coumestrol) from kudzu root could spontaneously bind with some core targets (CDK1 and CDC20), and cell experiments demonstrated that the extract from Puerariae Lobatae Radix could effectively inhibit the proliferation of HepG2 liver cancer cells. This study may provide a reference for the research and development of Puerariae Lobatae Radix and offer a theoretical basis for the discovery of its anti-HCC active ingredients.