Exploring the mechanism of action of Bidens pilosa L. in combating hepatic fibrosis through network pharmacology and molecular docking: An observational study.

Based on network pharmacology and molecular docking methods, to explore the possible targets and mechanisms of Bidens pilosa L. in treatment of liver fibrosis. The TCMSP, GeneCard, OMIM, TTD and DrugBank databases were used to obtain the targets of Bidens pilosa L and liver fibrosis, than the intersection targets were screened out by Venny 2.1.0, the protein-protein interaction (PPI) network and the core targets were obtained by the STRING database. Use Cytoscape3.7.2 software to draw the "traditional Chinese medicine-component-target-disease" network. The DAVID database platform was explored to analyze the biological process and pathway, and predict the anti-liver fibrosis mechanism of Bidens pilosa L. AutoDock and PyMol were used to verify the molecular docking between the active ingredients of Bidens pilosa L. and the core targets. Six active components of Bidens pilosa L. and 106 intersection targets were screened. PIK3R1, HSP90AA1, SRC, TP53, AKT1, RELA and other core targets were screened by PPI network analysis. The results of GO and KEGG enrichment analysis showed that the anti-liver fibrosis of Bidens pilosa L mainly involved in the regulation and negative regulation of apoptosis process, positive regulation of protein kinase B signal transduction, positive regulation of cell migration and other biological processes. Pathways acting on cancer, fluid shear stress and atherosclerosis, lipids and atherosclerosis, PI3K-AKT signaling pathway, MAPK signaling pathway and other signaling pathways. Molecular docking showed that the active components of Bidens pilosa L. displayed good binding activity with core target proteins, and the average binding energy was -7.47 kcal/mol. The possible mechanism of the active components against liver fibrosis is to regulate the PI3K-AKT, MAPK, and other signaling pathways by acting on core targets such as PIK3R1, HSP90AA1, SRC, TP53, AKT1, RELA, and induce the apoptosis of activated HSC cells to reverse and improve liver fibrosis.

A real-world analysis of safety profile of selexipag by using FDA adverse Event Reporting System (FAERS).

BACKGROUND: The current investigation sought to conduct a real-world analysis of adverse events (AEs) associated with selexipag by utilizing data from the Food and Drug Administration Adverse Event Reporting System (FAERS). METHODS: The Reporting Odds Ratios (ROR) and the Medicines Healthcare Products Regulatory Agency (MHRA) method were employed to assess the potential associations between selexipag and AEs. Case reports of adverse drug reaction (ADR) related to selexipag were systematically sourced from PubMed, Embase, and Web of Science databases. RESULTS: Our analysis identified 281 Preferred Terms (PTs) signals across 20 System Organ Classes (SOCs) were found to meet the screening threshold. The most common AEs were consistent with instructions, randomized controlled trials (RCTs), and case reports. Of significant note, unexpected AEs principally target SOCs of infections and infestations, blood and lymphatic system, renal and urinary disorders, hepatobiliary disorders, including pneumonia, metapneumovirus, decreased hemoglobin. transfusion, iron-deficiency anemia, dialysis hypotension, abnormal creatinine renal clearance, liver function test increased, hepatic function abnormal, hepatic enzyme increased. Within the pediatric population, unexpected signals such as pyrexia, pneumonia, and intussusception necessitate special precautionary measures. CONCLUSIONS: The findings contribute valuable insights to clinical practice, reinforcing the importance of vigilant monitoring, and can be instrumental in guiding both therapeutic applications and safety assessments of this particular medication.