Background: To explore the active ingredients, prospective targets, and action mechanisms of SanShi ShengXin Ointment in the treatment of pressure ulcers (PU) based on the network pharmacology technique and molecular docking technology.
Methods: The active ingredients and action targets of Sanshishengxin Ointment were searched through the Traditional Chinese Medicine Systematic Pharmacology Database and Analysis Platform. The PU-related targets were retrieved from the GeneCards and DisGeNET databases. The intersection target genes of disease and drugs were obtained. The "disease-drug-active ingredient-target" was constructed using Cytoscape software. The intersection target genes were imported into the String database to construct a protein-protein interaction network for gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses. The Auto Dock software was used for relevant molecular docking.
Results: A total of 78 active ingredients of SanShi ShengXin Ointment were obtained, corresponding to 539 target genes. There were 5896 PU-related target genes, and 373 intersection target genes of disease and drugs were obtained, such as STAT3, TP53, JUN, MAPK3, CTNNB1, involving PI3K-Akt, TNF, MAPK, and other related signaling pathways.
Conclusion: Based on network pharmacology and molecular docking analyses, this study demonstrates that SanShi ShengXin Ointment can treat PU through multicomponent, multitarget, and multipathway. .
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http://dx.doi.org/10.1097/MD.0000000000037390 | DOI Listing |
Viruses
December 2024
Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, 117997 Moscow, Russia.
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December 2024
Division of Virology, ICMR-National Institute of Translational Virology and AIDS Research, Pune 411026, MH, India.
Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (KSHV), which are the only members of the gamma(γ) herpesviruses, are oncogenic viruses that significantly contribute to the development of various human cancers, such as Burkitt's lymphoma, nasopharyngeal carcinoma, Hodgkin's lymphoma, Kaposi's sarcoma, and primary effusion lymphoma. Oncogenesis triggered by γ-herpesviruses involves complex interactions between viral genetics, host cellular mechanisms, and immune evasion strategies. At the genetic level, crucial viral oncogenes participate in the disruption of cell signaling, leading to uncontrolled proliferation and inhibition of apoptosis.
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December 2024
Department of Biological Sciences, University of Toledo, 2801 West Bancroft Street, Toledo, OH 43606, USA.
During virus infection, the activation of the antiviral endoribonuclease, ribonuclease L (RNase L), by a unique ligand 2'-5'-oilgoadenylate (2-5A) causes the cleavage of single-stranded viral and cellular RNA targets, restricting protein synthesis, activating stress response pathways, and promoting cell death to establish broad antiviral effects. The immunostimulatory dsRNA cleavage products of RNase L activity (RL RNAs) recruit diverse dsRNA sensors to activate signaling pathways to amplify interferon (IFN) production and activate inflammasome, but the sensors that promote cell death are not known. In this study, we found that DEAH-box polypeptide 15 (DHX15) and retinoic acid-inducible gene I (Rig-I) are essential for apoptosis induced by RL RNAs and require mitochondrial antiviral signaling (MAVS), c-Jun amino terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38 MAPK) for caspase-3-mediated intrinsic apoptosis.
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November 2024
Department of Microbiology, University of Washington School of Medicine, Seattle, WA 98109, USA.
Certain species D human adenoviruses (HAdV-D19, -D37, and -D64) are causative agents of epidemic keratoconjunctivitis. HAdV-D37 has previously been shown to bind CD46 (membrane cofactor protein) and sialic acid as adhesion receptors. HAdV-D64 is genetically highly similar to HAdV-D37, with an identical fiber protein sequence, but differs substantially in its penton base and hexon proteins, two other major capsid components, due to genetic recombination.
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November 2024
Istituto Zooprofilattico Sperimentale del Lazio e della Toscana "M. Aleandri", Via Appia Nuova 1411, 00178 Rome, Italy.
The mechanisms of the innate immunity control of equine infectious anemia virus in horses are not yet widely described. Equine monocytes isolated from the peripheral blood of three Equine infectious anemia (EIA) seronegative horses were differentiated in vitro into macrophages that gave rise to mixed cell populations morphologically referable to M1 and M2 phenotypes. The addition of two equine recombinant cytokines and two EIA virus reference strains, Miami and Wyoming, induced a more specific cell differentiation, and as for other species, IFNγ and IL4 stimulation polarized horse macrophages respectively towards the M1 and the M2 phenotypes.
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