scholarly journals The Key Genes Underlying Pathophysiology Association between Plaque Instability and Progression of Myocardial Infarction

2021 ◽  
Vol 2021 ◽  
pp. 1-19
Author(s):  
Yue Zheng ◽  
Yijie Gong ◽  
Yuheng Lang ◽  
Zhenchang Qi ◽  
Xiaomin Hu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Young Patients ◽  
Mapk Signaling ◽  
Venn Diagram ◽  
Pathway Enrichment Analysis ◽  
Leukocyte Activation ◽  
Hub Genes ◽  
Aged Mice ◽  
Increased Risk ◽  
Young Mice

Young patients with type 2 diabetes and myocardial infarction (MI) have higher long-term all-cause and cardiovascular mortality. In addition, the observed increased, mildly abnormal baseline lipid levels, but not lipid variability, are associated with an increased risk of atherosclerotic cardiovascular disease events, particularly MI. This study investigated differentially expressed genes (DEGs), which might be potential targets for young patients with MI and a high-fat diet (HFD). GSE114695 and GSE69187 were downloaded and processed using the limma package. A Venn diagram was applied to identify the same DEGs, and further pathway analysis was performed using Metascape. Protein-protein interaction (PPI) network analysis was then applied, and the hub genes were screened out. Pivotal miRNAs were predicted and validated using the miRNA dataset in GSE114695. To investigate the cardiac function of the screened genes, an MI mouse model, echocardiogram, and ELISA of hub genes were applied, and a correlation analysis was also performed. From aged mice fed HFD, 138 DEGs were extracted. From aged mice fed with chow, 227 DEGs were extracted. Pathway enrichment analysis revealed that DEGs in aging mice fed HFD were enriched in lipid transport and lipid biosynthetic process 1 d after MI and in the MAPK signaling pathway at 1 w after MI, suggesting that HFD has less effect on aging with MI. A total of 148 DEGs were extracted from the intersection between plaques fed with HFD and chow in young mice and MI_1d, respectively, which demonstrated increased inflammatory and adaptive immune responses, in addition to myeloid leukocyte activation. A total of 183 DEGs were screened out between plaques fed with HFD vs. chow in young mice and MI_1w, respectively, which were mainly enriched in inflammatory response, cytokine production, and myeloid leukocyte activation. After validation, PAK3, CD44, CD5, SOCS3, VAV1, and PIK3CD were demonstrated to be negatively correlated with LVEF; however, P2RY1 was demonstrated to be positively correlated. This study demonstrated that the screened hub genes may be therapeutic targets for treating STEMI patients and preventing MI recurrence, especially in young MI patients with HFD or diabetes.

scholarly journals PIK3R1, SPNB2, and CRYAB as Potential Biomarkers for Patients with Diabetes and Developing Acute Myocardial Infarction

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Yue Zheng ◽  
Yuheng Lang ◽  
Zhenchang Qi ◽  
Wenqing Gao ◽  
Xiaomin Hu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Young Patients ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Venn Diagram ◽  
Hub Genes ◽  
Ventricular Ejection Fraction ◽  
Pathway Analyses ◽  
Potential Biomarkers

Background. Young patients with type 2 diabetes mellitus (DM) and acute myocardial infarction (AMI) have high long-term all-cause and cardiovascular mortality rates. We aimed to investigate the differentially expressed genes (DEGs) that might be potential targets for DM patients with AMI. Methods. Gene datasets GSE775, GSE19322, and GSE97494 were meta-analyzed to obtain DEGs of the left ventricle myocardium in infarcted mice. Gene datasets including GSE3313, GSE10617, and GSE136948 were meta-analyzed to identify DEGs in diabetes mice. A Venn diagram was used to obtain the overlapping DEGs. KEGG and GO pathway analyses were performed, and hub genes were obtained. Pivotal miRNAs were predicted and validated using the miRNA dataset in GSE114695. To investigate the cardiac function of the screened genes, a MI mouse model was constructed; echocardiogram, qPCR, and ELISA of hub genes were performed; ELISA of hub genes in human blood samples was also utilized. Results. A total of 67 DEGs were identified, which may be potential biomarkers for patients with DM and AMI. GO and KEGG pathway analyses were performed, which were mainly enriched in response to organic cyclic compound and PI3K-Akt signaling pathway. The expression of PIK3R1 and SPNB2 increased in the MI group and was negatively correlated to left ventricular ejection fraction (LVEF), whereas that of CRYAB decreased and was positively correlated to LVEF. Patients with high CRYAB expression demonstrated a short hospital stay and the area under the curves of the three protein levels before and after treatment were 0.964, 0.982, and 0.918, suggesting that PIK3R1, SPNB2, and CRYAB may be diagnostic and prognostic biomarkers for the diabetes patients with AMI. Conclusion. The screened hub genes, PIK3R1, SPNB2, and CRYAB, were validated as credible molecular biomarkers and may provide a novel therapy for diabetic cardiac diseases with increased proteotoxic stress.

scholarly journals Anticancer Effects of Emodin on HepG2 Cell: Evidence from Bioinformatic Analysis

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Rui-sheng Zhou ◽  
Xiong-Wen Wang ◽  
Qin-feng Sun ◽  
Zeng Jie Ye ◽  
Jian-wei Liu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Hepg2 Cells ◽  
Molecular Mechanisms ◽  
Mapk Signaling ◽  
Ion Concentration ◽  
Receptor Interaction ◽  
Pathway Enrichment Analysis ◽  
Mrna Levels ◽  
Hub Genes ◽  
Positive Regulation

Hepatocellular carcinoma (HCC) is a primary cause of cancer-related death in the world. Despite the fact that there are many methods to treat HCC, the 5-year survival rate of HCC is still at a low level. Emodin can inhibit the growth of HCC cells invitroand invivo. However, the gene regulation of emodin in HCC has not been well studied. In our research, RNA sequencing technology was used to identify the differentially expressed genes (DEGs) in HepG2 cells induced by emodin. A total of 859 DEGs were identified, including 712 downregulated genes and 147 upregulated genes in HepG2 cells treated with emodin. We used DAVID for function and pathway enrichment analysis. The protein-protein interaction (PPI) network was constructed using STRING, and Cytoscape was used for module analysis. The enriched functions and pathways of the DEGs include positive regulation of apoptotic process, structural molecule activity and lipopolysaccharide binding, protein digestion and absorption, ECM-receptor interaction, complement and coagulation cascades, and MAPK signaling pathway. 25 hub genes were identified and pathway analysis revealed that these genes were mainly enriched in neuropeptide signaling pathway, inflammatory response, and positive regulation of cytosolic calcium ion concentration. Survival analysis showed that LPAR6, C5, SSTR5, GPR68, and P2RY4 may be involved in the molecular mechanisms of emodin therapy for HCC. A quantitative real-time PCR (qRT-PCR) assay showed that the mRNA levels of LPAR6, C5, SSTR5, GPR68, and P2RY4 were significantly decreased in HepG2 cells treated with emodin. In conclusion, the identified DEGs and hub genes in the present study provide new clues for further researches on the molecular mechanisms of emodin.

scholarly journals Network Pharmacology Identifies the Mechanisms of Sang-Xing-Zhi-Ke-Fang against Pharyngitis

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Yinhe Deng ◽  
Quanjiang Li ◽  
Menglin Li ◽  
Tiantian Han ◽  
Guixian Li ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Influenza A ◽  
Molecular Mechanisms ◽  
Mapk Signaling ◽  
Venn Diagram ◽  
Network Pharmacology ◽  
Pathway Enrichment Analysis ◽  
Ras Signaling ◽  
Clinical Effects ◽  
Overlapping Genes

Background. Sang-Xing-Zhi-Ke-Fang (SXZKF) demonstrates good therapeutic effect against pharyngitis. Nevertheless, the pharmacological mechanism underlying its effectiveness is still unclear. Objective. To investigate the underlying mechanisms of SXZKF against pharyngitis using network pharmacology method. Methods. Bioactive ingredients of SXZKF were collected and screened using published literature and two public databases. Using four public databases, the overlapping genes between these bioactive compound-related and pharyngitis-related genes were identified by Venn diagram. Protein-protein interaction (PPI) was obtained using “Search Tool for the Retrieval of Interacting Genes (STRING)” database. “Database for Annotation, Visualization, and Integrated Discovery ver. 6.8 (DAVID 6.8)” was used to perform Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis to explore the molecular mechanisms of SXZKF against pharyngitis. Finally, Cytoscape 3.7.2 software was used to construct and visualize the networks. Result. A total of 102 bioactive compounds were identified. Among them, 886 compounds-related and 6258 pharyngitis-related genes were identified, including 387 overlapping genes. Sixty-three core targets were obtained, including ALB, PPARγ, MAPK3, EGF, and PTGS2. Signaling pathways closely related to mechanisms of SXZKF for pharyngitis were identified, including serotonergic synapse, VEGF signaling pathway, Fc epsilon RI signaling pathway, Ras signaling pathway, MAPK signaling pathway, and influenza A. Conclusion. This is the first identification of in-depth study of SXZKF against pharyngitis using network pharmacology. This new evidence could be informative in providing new support on the clinical effects of SXZKF on pharyngitis and for the development of personalized medicine for pharyngitis.

A 16-year-old with ST elevation myocardial infarction: case report and review of the literature

2015 ◽  
Vol 26 (2) ◽  
pp. 230-236 ◽  
Author(s):  
Dustin Hill ◽  
Adam Waldman ◽  
Deepak Vivek
Keyword(s):  
Risk Factors ◽  
Myocardial Infarction ◽  
Young Adults ◽  
Chest Pain ◽  
Young Patients ◽  
St Elevation Myocardial Infarction ◽  
Laboratory Evaluation ◽  
Uneventful Recovery ◽  
Increased Risk ◽  
St Elevation

AbstractChest pain in young adults presents a unique diagnostic challenge, placing young patients at an increased risk to be misdiagnosed, as this patient population typically does not demonstrate the traditional risk factors associated with cardiovascular disease. This study details the case of a 16-year-old male who presented with new-onset chest pain and ST elevation on electrocardiogram. His history was unremarkable for known cardiac risk factors, but laboratory evaluation demonstrated markedly elevated troponins and electrocardiographic findings confirmed ST-segment elevation myocardial infarction. Coronary angiography demonstrated 100% occlusion of the left anterior descending artery, which was managed with percutaneous transluminal coronary angioplasty, thrombectomy, and bare-metal stenting. The patient had an uneventful recovery. This study examines the major causes of ST elevation myocardial infarction in young adults and reviews the major differences between younger and older myocardial infarction populations with emphasis on risk factor profile, pathophysiological mechanisms, clinical presentation, angiographic findings, and prognosis. This review highlights the need for consideration of a wide differential in younger subsets of the population presenting with chest pain and ST elevation. The implementation of current adult management protocols and guidelines for ST elevation myocardial infarction should not be overlooked due to age. Given the potential for premature death and long-term disability with resulting individual and societal consequences, it is crucial to understand the importance of correct diagnostic evaluation in this clinical scenario.

scholarly journals Microarray Data Mining and Preliminary Bioinformatics Analysis of Hepatitis D Virus-Associated Hepatocellular Carcinoma

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Zhe Yu ◽  
Xuemei Ma ◽  
Wei Zhang ◽  
Xiujuan Chang ◽  
Linjing An ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Cycle ◽  
The Cancer Genome Atlas ◽  
Venn Diagram ◽  
Pathway Enrichment Analysis ◽  
Ppi Network ◽  
Hepatitis D ◽  
Increased Risk ◽  
Key Genes

Several studies have demonstrated that chronic hepatitis delta virus (HDV) infection is associated with a worsening of hepatitis B virus (HBV) infection and increased risk of hepatocellular carcinoma (HCC). However, there is limited data on the role of HDV in the oncogenesis of HCC. This study is aimed at assessing the potential mechanisms of HDV-associated hepatocarcinogenesis, especially to screen and identify key genes and pathways possibly involved in the pathogenesis of HCC. We selected three microarray datasets: GSE55092 contains 39 cancer specimens and 81 paracancer specimens from 11 HBV-associated HCC patients, GSE98383 contains 11 cancer specimens and 24 paracancer specimens from 5 HDV-associated HCC patients, and 371 HCC patients with the RNA-sequencing data combined with their clinical data from the Cancer Genome Atlas (TCGA). Afterwards, 948 differentially expressed genes (DEGs) closely related to HDV-associated HCC were obtained using the R package and filtering with a Venn diagram. We then performed gene ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis to determine the biological processes (BP), cellular component (CC), molecular function (MF), and KEGG signaling pathways most enriched for DEGs. Additionally, we performed Weighted Gene Coexpression Network Analysis (WGCNA) and protein-to-protein interaction (PPI) network construction with 948 DEGs, from which one module was identified by WGCNA and three modules were identified by the PPI network. Subsequently, we validated the expression of 52 hub genes from the PPI network with an independent set of HCC dataset stored in the Gene Expression Profiling Interactive Analysis (GEPIA) database. Finally, seven potential key genes were identified by intersecting with key modules from WGCNA, including 3 reported genes, namely, CDCA5, CENPH, and MCM7, and 4 novel genes, namely, CDC6, CDC45, CDCA8, and MCM4, which are associated with nucleoplasm, cell cycle, DNA replication, and mitotic cell cycle. The CDCA8 and stage of HCC were the independent factors associated with overall survival of HDV-associated HCC. All the related findings of these genes can help gain a better understanding of the role of HDV in the underlying mechanism of HCC carcinogenesis.

scholarly journals Exploring the Pharmacological Mechanism of Duhuo Jisheng Decoction in Treating Osteoporosis Based on Network Pharmacology

2021 ◽  
Vol 2021 ◽  
pp. 1-21
Author(s):  
Zhencheng Xiong ◽  
Can Zheng ◽  
Yanan Chang ◽  
Kuankuan Liu ◽  
Li Shu ◽  
...  
Keyword(s):  
Molecular Docking ◽  
Signaling Pathway ◽  
Enrichment Analysis ◽  
Mapk Signaling ◽  
Network Pharmacology ◽  
Pathway Enrichment Analysis ◽  
Hub Genes ◽  
Active Compounds ◽  
Treatment Of Osteoporosis ◽  
Target Proteins

Objective. The purpose of this work is to study the mechanism of action of Duhuo Jisheng Decoction (DHJSD) in the treatment of osteoporosis based on the methods of bioinformatics and network pharmacology. Methods. In this study, the active compounds of each medicinal ingredient of DHJSD and their corresponding targets were obtained from TCMSP database. Osteoporosis was treated as search query in GeneCards, MalaCards, DisGeNET, Therapeutic Target Database (TTD), Comparative Toxicogenomics Database (CTD), and OMIM databases to obtain disease-related genes. The overlapping targets of DHJSD and osteoporosis were identified, and then GO and KEGG enrichment analysis were performed. Cytoscape was employed to construct DHJSD-compounds-target genes-osteoporosis network and protein-protein interaction (PPI) network. CytoHubba was utilized to select the hub genes. The activities of binding of hub genes and key components were confirmed by molecular docking. Results. 174 active compounds and their 205 related potential targets were identified in DHJSD for the treatment of osteoporosis, including 10 hub genes (AKT1, ALB, IL6, MAPK3, VEGFA, JUN, CASP3, EGFR, MYC, and EGF). Pathway enrichment analysis of target proteins indicated that osteoclast differentiation, AGE-RAGE signaling pathway in diabetic complications, Wnt signaling pathway, MAPK signaling pathway, PI3K-Akt signaling pathway, JAK-STAT signaling pathway, calcium signaling pathway, and TNF signaling pathway were the specifically major pathways regulated by DHJSD against osteoporosis. Further verification based on molecular docking results showed that the small molecule compounds (Quercetin, Kaempferol, Beta-sitosterol, Beta-carotene, and Formononetin) contained in DHJSD generally have excellent binding affinity to the macromolecular target proteins encoded by the top 10 genes. Conclusion. This study reveals the characteristics of multi-component, multi-target, and multi-pathway of DHJSD against osteoporosis and provides novel insights for verifying the mechanism of DHJSD in the treatment of osteoporosis.

scholarly journals Acute myocardial infarction,arterial thrombosis and thrombophilia in young patients

2020 ◽  
Vol 26 (4) ◽  
pp. 26-39
Author(s):  
Ivo Petrov ◽  
Naydenka Zlatareva-Gronkova ◽  
Todor Kundurdjiev ◽  
Viktoria Dimitrova
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Arterial Thrombosis ◽  
Young Patients ◽  
Specific Treatment ◽  
Premature Coronary Artery Disease ◽  
Thrombotic Risk ◽  
Coronary Syndrome ◽  
Increased Risk ◽  
Blood Coagulation Abnormality

Acute coronary syndrome (ACS) represent emergency state in an intensive cardiovascular care unit, which implies immediate and specific treatment. Of peculiar interest for cardiologists are young patients with acute myocardial infarction (AMI). The family history taking for premature coronary artery disease (CAD) and establishment of genetic factors, responsible for coagulation, both are on target for this group of patients. Gold standard for AMI diagnosis is coronary angiography (CA), which usually implies endovascular treatment (EVT). When coronary thrombus formation is found in young patients, different diagnostic opportunities are possible. Thrombophilia (TF) represents blood coagulation abnormality resulting in an increased risk of thrombosis. It could affect different sections of the cardiovascular system, most commonly venous, but also arterial. This clinical condition could be confirmed by performing laboratory genetic tests. We studied a group of forty-one young patients with first appearance of ACS ≤ 55 years old included for a five-year period. All of them were evaluated with CA and received EVT. According to the thrombotic risk, we defined a high-risk group, treated with anticoagulant (AC) on top of dual antiplatelet therapy (DAPT). The patients were followed-up for recurrent ischemic and bleeding events. We performed laboratory tests for the most frequent TF gene mutations in Bulgarian population. There is a conflicting data about this issue in different ethnic origins. The aim of our study is to estimate the possible relationship between the TF and the arterial thrombosis in young ACS patients, to defi ne specific treatment strategies, improving the prognosis of the patients.

scholarly journals Evaluation of serum homocysteine in young patients presenting with myocardial infarction: a study from rural Maharashtra

2020 ◽  
Vol 7 (11) ◽  
pp. 1635
Author(s):  
Sudam V. Khedkar ◽  
Sudeep Kumar ◽  
Praveen Patil ◽  
Anant A. Takalkar
Keyword(s):  
Myocardial Infarction ◽  
Heart Disease ◽  
Elevated Serum ◽  
Young Patients ◽  
Study Cohort ◽  
Case Control Studies ◽  
Cross Sectional ◽  
Male Predominance ◽  
Serum Homocysteine ◽  
Increased Risk

Background: It has been shown that elevated serum homocysteine levels are associated with an increased risk of ischemic heart disease (IHD) and stroke. Also, higher homocysteine concentrations in IHD or stroke patients than in controls have been reported. Some prospective and case-control studies with inconsistent results, some with highly significant results and others with no association have been observed. Objective of the study was to evaluate the serum homocysteine level in young myocardial infarction patients of rural hospital.Methods: The present hospital based cross sectional observational study was carried out in Department of Medicine, MIMER Medical College and Hospital, Talegaon Dabhade, Pune. The study population included 45 young patients having acute myocardial Infarction coming to our hospital. The data thus collected was entered in MS excel sheet and analysed by using SPSS 24.0 IBM USA.Results: Mean age of the study cohort was 36.7 years with 48.9% cases in between the age of 31-40 years and 33.3% were in the age range of 41-45 years. Male predominance was seen in the study cases with 68.9% males and 31.1% females. Prevalence of hyperhmocysteinemia was observed as 64.4% in present study. Mortality rate in our study was 6.67%. Serum homocysteine and all lipid parameters were in positive correlation except High-density lipoprotein which has negative correlation. Homocysteine levels were correlating significantly with level of atherosclerosis as measured by Gensini score.Conclusions: Coronary heart disease is related to high serum homocysteine concentration. Serum homocysteine levels also correlates well with the severity of MI.

scholarly journals A novel murine model of multi-day moderate ethanol exposure reveals increased intestinal dysfunction and liver inflammation with age

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Rachel H McMahan ◽  
Kevin M Najarro ◽  
Juliet E Mullen ◽  
Madison T Paul ◽  
David J Orlicky ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alcohol Use ◽  
Murine Model ◽  
Ethanol Exposure ◽  
Alcoholic Beverages ◽  
Liver Inflammation ◽  
Aged Mice ◽  
Increased Risk ◽  
Junction Protein ◽  
Young Mice

Abstract Background There are currently > 600 million people over the age of 65 globally and this number is expected to double by the year 2050. Alcohol use among this population is on the rise, which is concerning as aging is associated with increased risk for a number of chronic illnesses. As most studies investigating the effects of alcohol have focused on young/middle-aged populations, there is a dearth of information regarding the consequences of alcohol use in older consumers. In addition, most murine ethanol models have concentrated on exposure to very high levels of ethanol, while the vast majority of elderly drinkers do not consume alcohol in excess; instead, they drink on average 2 alcoholic beverages a day, 3–4 days a week. Methods We designed a murine model of aging and moderate ethanol consumption to determine if the deleterious effects of alcohol on the gut-liver axis are exacerbated in aged, relative to younger, animals. Aged and young mice were exposed to a multi-day moderate exposure ethanol regimen for 4 weeks and changes in gut permeability along with intestinal tight junction protein and antimicrobial peptide gene expression were measured. In addition, hepatic inflammation was assessed by histological analysis, inflammatory gene expression and flow cytometric analysis of inflammatory infiltrate. Results Our results reveal that in aged, but not young mice, moderate ethanol exposure yielded significantly worsened intestinal permeability, including increased bacterial translocation from the gut, elevated serum iFABP and leakage of FITC-dextran from the gut. Interestingly, moderate ethanol exposure in young animals led to gut protective transcriptional changes in the ileum while this protective response was blunted in aged mice. Finally, moderate ethanol exposure in aged mice also resulted in marked inflammatory changes in the liver. Conclusions These results demonstrate that aged mice are more susceptible to ethanol-induced gut barrier dysfunction and liver inflammation, even at moderate doses of ethanol. This increased vulnerability to ethanol’s gastrointestinal effects has important implications for alcohol use in the aging population. Future studies will explore whether improving intestinal barrier function can reverse these age-related changes.

scholarly journals Network Pharmacology-Based Prediction of Active Ingredients and Mechanisms of Tongxinluo Against Acute Myocardial Infarction

2021 ◽  
Author(s):  
Meng-Jin Hu ◽  
Gui-Hao Chen ◽  
Yue-Jin Yang
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Scientific Evidence ◽  
Interaction Network ◽  
Enrichment Analysis ◽  
Venn Diagram ◽  
Network Pharmacology ◽  
Pathway Enrichment Analysis ◽  
Overlapping Genes ◽  
Active Ingredients

Abstract Purpose: The aim of this network pharmacology was to explore the potential active ingredients and mechanisms of Tongxinluo (TXL) against acute myocardial infarction (AMI).Methods: We selected active ingredients and targets of TXL according to TCMSP database and converted protein targets into gene symbol by UniProt database. Therapeutic gene targets on AMI were collected from DisGeNET and GeneCards databases. The overlapping genes between ingredients and AMI were identified using Venn diagram. Then, the interaction network between ingredients and overlapping genes was constructed, visualized, and analyzed by Cytoscape software. Protein-protein interaction (PPI) was analyzed by String database. Finally, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of overlapping genes were carried out by metascape platform.Results: A total of 111 active ingredients, 184 ingredient-related genes, and 1020 AMI-related genes were retrieved using public databases. Eventually, 79 overlapping genes between TXL and AMI were identified. Cytoscape and PPI results suggested that the active ingredients and genes of TXL against AMI consisted of 66 active ingredients and 79 genes, among them beta-sitosterol and IL-6 were the uppermost active ingredient and hub gene, respectively. Metascape results exhibited that the key mechanism of TXL against AMI might be reducing oxidative stress in cell membrane by inactivating pathways in cancer.Conclusion: This network pharmacology study reveals potential mechanisms of multi-target and multi-component TXL in the treatment of AMI, providing scientific evidence for further expounding the active ingredients and mechanisms of TXL against AMI.

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