Integrative Network Pharmacology and Molecular Docking-Based Validation of Berberine as a Therapeutic Agent in Arsenic-Induced Cardiotoxicity.

Objective Exploring the preventive and therapeutic effects of dapagliflozin (DAPA) on gouty arthritis (GA) in rats, and revealing its potential mechanism of action. Methods Potential targets of DAPA were identified from DrugBank, Swiss Target Prediction, CTD, and PharmMapper databases. Targets associated with gouty arthritis (GA) were retrieved from Gene Cards, DisGeNET, and NCBI databases. By taking the intersection of these two sets, common targets of DAPA and GA were determined. These common targets were then subjected to Gene Ontology (GO) functional annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Use the CB-DOCK2 online molecular docking platform to dock DAPA with the core target and perform visual analysis. Thirty-two SPF-grade male SD rats were randomly divided into four groups, with eight rats in each: a blank control group, a model group, a 20 mg/kg DAPA group, and a 40 mg/kg DAPA group. Rats received daily gavage administration of the corresponding medication for eight consecutive days. On the fifth day, monosodium urate (MSU) crystal suspension was injected into the left ankle joint to establish an acute GA model. Samples were collected one hour after the final gavage. The swelling of the ankle joints was recorded at various time points. Hematoxylin and eosin (HE) staining was used to observe pathological changes in the synovial tissue of the ankle joints. Enzyme-linked immunosorbent assay (ELISA) was conducted to measure the levels of inflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in the peripheral blood of the rats. Western blotting was performed to detect the expression levels of signaling pathway proteins in the synovial tissue of the ankle joints. Results Based on network pharmacology analysis and molecular docking, it was found that targets were significantly enriched in the nucleotide binding oligomerization domain (NOD)-like receptor (NLR) signaling pathway, and the binding energies between the related core targets and DAPA were all <-7.0 kcal/mol. In animal experiments, regarding ankle joint swelling: compared with the model group, the 20 mg/kg DAPA group showed a significant reduction in ankle joint swelling at 72 hours post-modeling (p<0.05), and the 40 mg/kg DAPA group exhibited significant reductions in ankle joint swelling at both 48 and 72 hours post-modeling (p<0.01). For ankle joint HE staining: compared with the model group, DAPA-treated groups showed varying degrees of attenuation in pathological damage, including inflammatory cell infiltration, synovial tissue proliferation, and vascular proliferation in the ankle joints. Peripheral blood ELISA results: the levels of IL-1β and TNF-α in DAPA-treated groups were significantly lower than those in the model group (p<0.05). As for the protein expression levels of NOD-like receptor thermal protein domain-associated protein 3 (NLRP3) and cysteinyl aspartate-specific proteinase-1 (Caspase-1) in ankle joint synovium: compared with the model group, the expression of NLRP3 and Caspase-1 proteins was significantly reduced in DAPA-treated groups (p<0.05). Conclusion DAPA may alleviate the inflammatory response in acute GA in rats by inhibiting the NLRP3/Caspase-1 pathway.

Sodium-glucose co-transporter 2 inhibitors (SGLT2is) have consistently been shown to be beneficial in reducing the incidence rate of coronary heart disease (CHD) in diabetic patients. However, their specific pharmacological mechanisms are still unknown. Therefore, we intend to explore the mechanism of SGLT2is in patients with type 2 diabetes mellitus (T2DM) combined with CHD through a network pharmacological approach. Firstly, the Swiss Target Prediction and Drugbank databases were used to predict the targets of SGLT2is. The CHD dataset GSE113079 and T2DM dataset GSE118139 were downloaded from the gene expression omnibus database, and the differentially expressed genes (DEGs) were analyzed. Then, the predicted targets of SGLT2is intersected with the DEGs of the two diseases, and the results were used to construct the “drug-targeted-disease (D-T-D)” and protein–protein interaction networks. Gene Ontology functional analyses and Kyoto Encyclopedia of Genes and Genomes pathway were used for functional studies of target genes. Finally, molecular docking of SGLT2i with target proteins was performed using AutoDockTools software, and the docking results were verified by ELISA, RT-qPCR and western-blot experiments. Among the drug targets of SGLT2is and DEGs in T2DM and CHD, a total of 14 common gene targets exist, and these genes mainly affect the disease progression through the “chemical carcinogenesis-reactive oxygen species”,“apoptosis,” and “chemical carcinogenesis-receptor activation” pathways. Through hub gene identification, we identified 11 hub genes from these 14 targets, of which epidermal growth factor receptor (EGFR) had the highest score. Molecular docking results showed that ertugliflozin had the strongest intermolecular binding to EGFR and that ertugliflozin improved the viability of high-glucose (HG)/high-lipid combined hypoxia-reoxygenation-injured (HG/HP + H/R) cardiomyocytes and inhibited EGFR expression in cardiomyocytes. Based on network pharmacology and bioinformatics analysis, our study elucidated that EGFR is the hub gene for T2DM combined with CHD myocardial injury. Molecular docking and cell experiments further confirmed that SGLT2i-ERTU improves HG/HP + H/R myocardial cell injury by targeting EGFR. Our study deepened the pharmacological mechanism of SGLT2is in the treatment of T2DM combined with CHD and provided a new perspective and therapeutic basis for future experimental research and healthcare.

The active components of honeysuckle alleviate smoke inhalation-induced lung injury by reducing inflammation and oxidative stress. This study aimed to investigate the intervention mechanism of honeysuckle blood components in smoke inhalation-induced lung injury using network pharmacology and molecular docking technology. The targets of honeysuckle blood-entering components were identified through the Swiss Target Prediction and Similarity Ensemble Approach databases. The target genes associated with smoke inhalation-induced lung injury were retrieved from the GeneCards and CTD databases. Cytoscape 3.7.1 software was employed to construct the blood component-target network of honeysuckle. GO biological process enrichment analysis of target genes related to inhalation-induced lung injury in Flos Lonicerae was performed using the DAVID tool. KEGG pathway enrichment analysis of anti-aspiration lung injury target genes in Flos Lonicera was conducted using the KOBAS 3.0 tool. The top six core targets with the highest PPIs in the network were selected for molecular docking verification. AutoDock was used to perform molecular docking with the blood-entering components of honeysuckle to verify their binding capabilities. A total of 95 targets of the blood components of honeysuckle and 960 targets related to smoke inhalation-induced lung injury were identified through network pharmacological analysis. Fifteen common targets of the blood components of honeysuckle were identified: CTSD, KLF5, TTR, HIF1A, CAPN1, GRIN1, ADAM10, ERAP1, NFE2L2, LGALS3, TLR4, GRB2, NF-κB1, RPS6KA1, and PTPN11. Network PPI analysis indicated that NF-κB1 was among the core targets. GO and KEGG enrichment analyses revealed that the components of Lonicerae lonicerae in the blood exerted therapeutic effects by regulating biological processes such as inflammation, apoptosis, oxidative stress, and the NF-κB signaling pathway. Molecular docking results showed that the blood components of honeysuckle exhibited strong binding affinities to IL-1β, NF-κB, and other core targets. This study revealed the potential mechanism of action of honeysuckle blood-entering components against smoke inhalation-induced lung injury through the NF-κB signaling pathway, NF-κB1, and other core targets, using network pharmacology and molecular docking techniques, thereby providing a theoretical foundation for further research on the application of honeysuckle in treating smoke inhalation-induced lung injury.

ZXGD Decoction, a traditional Chinese formulation historically used for cardiovascular ailments, was evaluated for its efficacy in coronary heart disease (CHD) through an integrated network pharmacology and randomized controlled trial (RCT) approach. Its selection was rooted in documented therapeutic benefits for blood stasis and endothelial dysfunction, with modern pharmacology identifying active compounds (e.g., luteolin, quercetin) targeting inflammation and oxidative stress pathways. Network analysis revealed ZXGD’s multi-target mechanism, prominently modulating the PI3K-AKT and NF-κB pathways, supported by robust molecular docking scores (binding affinity < -7.0 kcal/mol). These findings align with CHD pathophysiology, suggesting ZXGD disrupts critical inflammatory cascades. In a double-blind RCT (n = 180), ZXGD adjunct therapy significantly improved angina frequency (35% reduction vs. control, p < 0.01) and endothelial function (FMD increase: 2.8% ± 0.5 vs. 1.2% ± 0.4, p < 0.05) over 12 weeks, with no severe adverse events. This underscores ZXGD’s clinical potential as a safe complementary treatment. Notably, lipid profile enhancements (LDL-C reduction: 18.3% vs. 11.7%) correlated with predicted network targets, including LDLR and HMGCR. Our results bridge traditional use with mechanistic evidence, reinforcing ZXGD’s role in CHD management. While prior studies emphasize ZXGD’s anti-thrombotic effects, this work uniquely validates its anti-inflammatory and lipid-modulating properties, addressing gaps in understanding its systemic impact. Clinically, these findings advocate for ZXGD’s integration into CHD therapeutic protocols, particularly for patients with residual inflammatory risk.

Unraveling the active ingredients and molecular mechanisms of Buyi Xiaozheng decoction against ovarian cancer: An integrative approach combining UHPLC-QE-MS, network pharmacology, molecular docking, dynamics simulations, and experimental verification.

Investigating the therapeutic effects of paeoniflorin on atopic dermatitis and its potential pathogenesis through network pharmacology and in vivo and in vitro experiments.

Primary dysmenorrhea (PDM) is a prevalent menstrual disorder among women, often underreported and undertreated. Wen-Jing-Zhi-Tong Decoction (WJZTD), a patented Traditional Chinese Medicine (TCM) herbal decoction, has shown efficacy in treating PDM. However, the underlying therapeutic mechanism of WJZTD in PDM treatment remains to be elucidated. This study aimed to employ integrative pharmacology and experimental validation to investigate the potential therapeutic mechanisms of WJZTD in treating PDM. The bioactive compounds of WJZTD were identified by UPLC-Q-Exactive-Orbitrap MS/MS and GC-MS. Putative targets of WJZTD were obtained from Swiss Target Prediction, STITCH, and BATMAN-TCM databases. Known targets of PDM were retrieved from Gene Cards and Drug Bank databases. Protein-to-protein interactions were constructed to screen key targets using the STRING database. Subsequently, GO and KEGG pathway enrichment analyses were performed based on Metascape. Finally, a PDM rat model was established to validate the potential therapeutic mechanisms of WJZTD using Western Blot, PCR, and ELISA. 390 bioactive compounds in WJZTD were identified through UPLC-Q-Exactive- Orbitrap MS/MS and GC-MS. Network pharmacology revealed 7 key compounds with 20 targets and pathways that are crucial for WJZTD in treating PDM. Behavioral tests confirmed that WJZTD can effectively ameliorate menstrual pain in PDM. WJZTD also inhibited prostaglandin production, thereby relieving uterine smooth muscle contraction. The downregulation of the BDNF/TrkB/ERK/CREB signaling pathway, identified as the key target and pathway through network pharmacology, may be crucial to the anti-nociceptive and anti-inflammatory effects of WJZTD in treating PDM. This study provides the first comprehensive analysis of the key compounds, targets, and pathways of WJZTD, laying a solid foundation for future pharmacological studies on PDM. The anti-nociceptive and anti-inflammatory effect may be attributed to the downregulation of the BDNF/TrkB/ERK/CREB signaling pathway.

Glycyrrhiza Glabra Linn (GG), known as Yashtimadhu in Ayurveda, is traditionally used for managing Parinam Shula (peptic ulcer). Despite its known therapeutic benefits, its molecular mechanisms remain unexplored. This study investigates GG's pharmacological action using computational approaches like network pharmacology and molecular docking. Bioactive compounds of GG were retrieved from IMPPAT, TCMSP, and TCM databases. Predicted targets were obtained from Swiss Target Prediction and STITCH, while PU-related targets were collected from DisGeNet, OMIM, and Gene Cards. Common targets between GG and PU underwent GO and KEGG enrichment analysis, and networks were visualized using Cytoscape 3.10.1. Molecular docking and In Vitro studies were conducted for validation. Network analysis identified 29 phytochemicals and 157 common GG-PU target genes. Key hub genes, including IL6, TP53, AKT1, STAT3 and TNF, were involved in inflammation, apoptosis, and tissue repair. Pathway enrichment suggested GG's anti-PU effects via the PI3K-Akt pathway. Molecular docking confirmed strong binding affinities, supported by In Vitro studies. GG exerts anti-PU effects through multi-target interactions, particularly via the PI3K-Akt signaling pathway. Quercetin is the major phytoconstituent showing interactions with multiple PU-related targets and exhibited the highest binding affinity. However, further in vivo and clinical studies are required to validate its full therapeutic potential. The online version contains supplementary material available at 10.1007/s40203-025-00429-y.

With successful antiretroviral therapy, patients infected with the human immunodeficiency virus (HIV) are living longer; however, recent reports suggest increased rates of coronary heart disease (CHD) among HIV-infected patients,1 and cardiovascular disease has become an important cause of morbidity and mortality in this population.2 Increased CHD rates in the HIV population may relate to traditional risk factors, including advancing age, higher smoking rates, dyslipidemia, insulin resistance, and impaired glucose tolerance. Cardiovascular disease may also be due to nontraditional factors, including changes in body composition with loss of subcutaneous fat and/or accumulation of visceral fat in some patients, inflammation, and direct effects of the virus on the vasculature, as well as to direct effects of specific antiretroviral drugs. Important questions remain as to the pathogenesis, detection, and treatment of cardiovascular disease and related risk factors in HIV-infected patients. These questions concern, among other things, the design of adequate trials to determine CHD incidence and the utility of existing CHD guidelines for screening, prevention, treatment, and risk stratification. To ascertain the state of the science with respect to these and related questions, a multidisciplinary conference with interested HIV specialists, cardiologists, endocrinologists, primary care physicians, National Institutes of Health representatives, and patient advocates was convened June 28–30, 2007, in Chicago, Ill, and chaired by Drs Steven Grinspoon and Robert Eckel. The discussions focused on 6 areas of interest, each with its own working group, including the following: (1) the contribution of metabolic and anthropometric abnormalities to cardiovascular disease risk factors (chaired by Drs Carl Grunfeld and Donald Kotler); (2) the epidemiological evidence for cardiovascular disease and its relationship to highly active antiretroviral therapy (HAART; chaired by Drs Judy Currier and Jens Lundgren); (3) the effects of HIV infection and antiretroviral therapy on the heart and vasculature (chaired by Drs Michael Dube …

We have reached a limit in our ability to reduce the incidence of coronary heart disease (CHD) and cardiovascular disease (CVD) utilizing the traditional evaluation, prevention, and treatment strategies for the top five cardiovascular risk factors – hypertension, diabetes mellitus (DM), dyslipidemia, obesity, and smoking. Statistics show that approximately 50% of patients will have CHD or myocardial infarction (MI) despite “normal” levels of these five risk factors as traditionally defined. A more logical and in-depth understanding is required of these top risk factors, including the evaluation of a 24-hour ambulatory blood pressure monitoring (24-hour ABM), advanced lipid testing, and more sophisticated parameters to evaluate dysglycemia and visceral obesity with effects of adipokines and of the three finite vascular responses: inflammation, oxidative stress, and immune vascular dysfunction related to numerous internal and external vascular insults. Understanding translational cardiovascular medicine to correlate the CHD risk factors to the presence or absence of vascular injury and disease with noninvasive vascular testing will allow for early identification, prevention, and treatment of CHD and CVD.

Resveratrol is a potent phytochemical known for its potential in treating cardiometabolic multimorbidity. However, its underlying mechanisms remain unclear. Our study systematically investigates the effects of resveratrol on cardiometabolic multimorbidity and elucidates its mechanisms using network pharmacology and molecular docking techniques. We screened cardiometabolic multimorbidity-related targets using the OMIM, GeneCards, and DisGeNET databases, and utilized the DSigDB drug characterization database to predict resveratrol's effects on cardiometabolic multimorbidity. Target identification for resveratrol was conducted using the TCMSP, SymMap, DrugBank, Swiss Target Prediction, CTD, and UniProt databases. SwissADME and ADMETlab 2.0 simulations were used to predict drug similarity and toxicity profiles of resveratrol. Protein-protein interaction (PPI) networks were constructed using Cytoscape 3.9.1 software. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analyses were performed via the DAVID online platform, and target-pathway networks were established. Molecular docking validated interactions between core targets and resveratrol, followed by molecular dynamics simulations on the optimal core proteins identified through docking. Differential analysis using the GEO dataset validated resveratrol as a core target in cardiometabolic multimorbidity. A total of 585 cardiometabolic multimorbidity target genes were identified, and the predicted results indicated that the phytochemical resveratrol could be a major therapeutic agent for cardiometabolic multimorbidity. SwissADME simulations showed that resveratrol has potential drug-like activity with minimal toxicity. Additionally, 6703 targets of resveratrol were screened. GO and KEGG analyses revealed that the main biological processes involved included positive regulation of cell proliferation, positive regulation of gene expression, and response to estradiol. Significant pathways related to MAPK and PI3K-Akt signaling pathways were also identified. Molecular docking and molecular dynamics simulations demonstrated strong interactions between resveratrol and core targets such as MAPK and EGFR. This study predicts potential targets and pathways of resveratrol in treating cardiometabolic multimorbidity, offering a new research direction for understanding its molecular mechanisms. Additionally, it establishes a theoretical foundation for the clinical application of resveratrol.

Objective: To explore the potential mechanism of propofol in improving antidepressant-like behavior through network pharmacology and animal experimental validation, providing theoretical and experimental support for the development of novel antidepressant drugs based on propofol. Methods: 1. The targets of propofol and the disease targets of depression were screened through Swiss Target prediction, Super-pred, SEA, Drugbank, CTD, GeneCards, OMIM, and TTD databases. A protein-protein interaction (PPI) network was constructed, and the core targets were screened and visualized using CytoScape 3.10.2 software. Additionally, GO and KEGG enrichment analyses of the intersection targets were performed using the Metascape database. 2. Thirty male C57BL/6 mice were randomly divided into the CON group, LH model group, and PRO treatment group, with 10 mice in each group. The sucrose preference test, forced swim test, and tail suspension test were conducted to determine whether the depression model was successfully established and to assess the improvement effect of propofol on antidepressant-like behavior. 3. The pathological morphological changes of hippocampal neurons in the three groups of mice were observed through HE staining experiments. The expression of mGluR5 protein in the hippocampus was analyzed by Western blot. Results: 1. Network pharmacology analysis indicated that propofol may exert antidepressant effects by acting on core genes such as ALB, ESR1, NFKB1, HSP90AB1, and EGFR. These core target genes were mainly enriched in biological processes such as synaptic transmission and membrane potential regulation; they involved cellular components such as GABA receptor complexes and synaptic membranes; and they included molecular functions such as neurotransmitter receptor activity. Additionally, propofol may exert antidepressant effects through signaling pathways such as neuroactive ligand-receptor interaction, morphine addiction, and GABAergic synapse. 2. Compared with the CON group, the sucrose preference rate of mice in the LH model group significantly decreased, while the immobility time in the forced swim test and tail suspension test significantly increased. Compared with the LH model group, the sucrose preference rate of mice in the PRO treatment group significantly increased, and the immobility time significantly decreased. 3. The HE results showed that compared with the CON group, the number of neurons in the LH group decreased, with loose arrangement, pycnotic and deeply stained nuclei with blurred boundaries. However, the number of necrotic neurons in the PRO group significantly decreased. The Western blot results showed that compared with the CON group, the expression level of mGluR5 protein in the LH model group significantly increased, while it significantly decreased in the PRO treatment group compared with the LH model group. Conclusion: Propofol may exert antidepressant effects by regulating the expression of mGluR5, improving antidepressant-like behavior, and reducing hippocampal neuronal necrosis.

Background:At present, there was no evidence that any drugs other than lung transplantation can effectively treat Idiopathic Pulmonary Fibrosis (IPF). Ligusticum wallichii, or Chinese name Chuan xiong has been widely used in different fibrosis fields. Our aim is to use network pharmacology and molecular docking to explore the pharmacological mechanism of the Traditional Chinese medicine (TCM) Ligusticum wallichii to improve IPF.Materials and methods:The main chemical components and targets of Ligusticum wallichii were obtained from TCMSP, Swiss Target Prediction and Phammapper databases, and the targets were uniformly regulated in the Uniprot protein database after the combination. The main targets of IPF were obtained through Gencards, OMIM, TTD and DRUGBANK databases, and protein interaction analysis was carried out by using String to build PPI network. Metascape platform was used to analyze its involved biological processes and pathways, and Cytoscape3.8.2 software was used to construct “component-IPF target-pathway” network. And molecular docking verification was conducted through Auto Dock software.Results:The active ingredients of Ligusticum wallichii were Myricanone, Wallichilide, Perlolyrine, Senkyunone, Mandenol, Sitosterol and FA. The core targets for it to improve IPF were MAPK1, MAPK14, SRC, BCL2L1, MDM2, PTGS2, TGFB2, F2, MMP2, MMP9, and so on. The molecular docking verification showed that the molecular docking affinity of the core active compounds in Ligusticum wallichii (Myricanone, wallichilide, Perlolyrine) was <0 with MAPK1, MAPK14, and SRC. Perlolyrine has the strongest molecular docking ability, and its docking ability with SRC (−6.59 kJ/mol) is particularly prominent. Its biological pathway to improve IPF was mainly acted on the pathways in cancer, proteoglycans in cancer, and endocrine resistance, etc.Conclusions:This study preliminarily identified the various molecular targets and multiple pathways of Ligusticum wallichii to improve IPF.

Traditional treatments of cancer have faced various challenges, including toxicity, medication resistance, and financial burdens. On the other hand, bioactive phytochemicals employed in complementary alternative medicine have recently gained interest due to their ability to control a wide range of molecular pathways while being less harmful. As a result, we used a network pharmacology approach to study the possible regulatory mechanisms of active constituents of Cordia myxa for the treatment of liver cancer (LC). Active constituents were retrieved from the IMPPAT database and the literature review, and their targets were retrieved from the STITCH and Swiss Target Prediction databases. LC-related targets were retrieved from expression datasets (GSE39791, GSE76427, GSE22058, GSE87630, and GSE112790) through gene expression omnibus (GEO). The DAVID Gene Ontology (GO) database was used to annotate target proteins, while the Kyoto Encyclopedia and Genome Database (KEGG) was used to analyze signaling pathway enrichment. STRING and Cytoscape were used to create protein-protein interaction networks (PPI), while the degree scoring algorithm of CytoHubba was used to identify hub genes. The GEPIA2 server was used for survival analysis, and PyRx was used for molecular docking analysis. Survival and network analysis revealed that five genes named heat shot protein 90 AA1 (HSP90AA1), estrogen receptor 1 (ESR1), cytochrome P450 3A4 (CYP3A4), cyclin-dependent kinase 1 (CDK1), and matrix metalloproteinase-9 (MMP9) are linked with the survival of LC patients. Finally, we conclude that four extremely active ingredients, namely cosmosiin, rosmarinic acid, quercetin, and rubinin influence the expression of HSP90AA1, which may serve as a potential therapeutic target for LC. These results were further validated by molecular dynamics simulation analysis, which predicted the complexes with highly stable dynamics. The residues of the targeted protein showed a highly stable nature except for the N-terminal domain without affecting the drug binding. An integrated network pharmacology and docking study demonstrated that C. myxa had a promising preventative effect on LC by working on cancer-related signaling pathways.

Curcuma aromatica Salisb. rhizome (CASR) has multifunctional characteristics worldwide and a long history of use as a botanical drug with. Currently, it is often used clinically to treat coronary heart disease (CHD) caused by blood stasis syndrome. However, the therapeutic mechanism of CASR in the treatment of CHD remains poorly understood. In study, the main chemical constituents of CASR were analyzed using UPLC-Q-TOF-MS/MS. Then, its potential therapeutic mechanism against CHD was predicted. Subsequently, pharmacological evaluation was performed using CHD rat model. Finally, a lipidomics approach was applied to explore the different lipid metabolites to verify the regulation of CASR on lipid metabolism disorders in CHD. A total of 35 compounds was identified from CASR. Seventeen active components and 51 potential targets related to CHD were screened by network pharmacology, involving 13 key pathways. In vivo experiments showed that CASR could significantly improve myocardial infarction, blood stasis, and blood lipid levels and regulate the PI3K/AKT/mTOR signaling pathway in CHD rats. Lipidomics further showed that CASR could regulate abnormal sphingolipid, glycerophospholipid, and glycerolipid metabolism in CHD rats. The therapeutic mechanism of CASR against CHD was initially elucidated and included the regulation of lipid metabolism. Its effects may be attributed to active ingredients, such as curzerene, isoprocurcumenol, and (+)-curcumenol. This study reveals the characteristics of multi-component and multi-pathway of CASR in the treatment of CHD, which provides a basis for the follow-up development and utilization of CASR.