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Dual Checkpoint Inhibition in M2 Macrophages via Anti-PD-L1 and siRNA-Loaded M1-Exosomes: Enhancing Tumor Immunity through RNA-Targeting Strategies.
Eur J Pharmacol
January 2025
Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran; Research Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran; Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education Research Network (USERN), Tehran, Iran. Electronic address:
The interaction between a cluster of differentiation 47 (CD47) on cancer cells and signal regulatory protein alpha (SIRPα) on macrophages is thought to hinder macrophage phagocytic activity, which can be blocked by combining siRNAs targeting SIRPα (siSIRPα) with simultaneous involvement of activating receptors like FcRs (Fc receptors) anti-programmed death-ligand 1 (anti-PD-L1). For this study, M1 macrophage-derived exosomes were used to deliver the siRNAs, isolated from lipopolysaccharide (LPS)-stimulated RAW264.7 cells and electroporated with siSIRPα.
View Article and Find Full Text PDFUSP25 stabilizes STAT6 to promote IL-4-induced macrophage M2 polarization and fibrosis.
Int J Biol Sci
January 2025
Department of Respiratory and Critical Care Medicine, National Clinical Research Center of Respiratory Disease, Key Laboratory of Pulmonary Diseases of Health Ministry, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
As a leading cause of morbidity and mortality, fibrosis is the common pathway of various chronic inflammatory diseases in organs and causes death in a large number of patients. It can destroy the structure and function of organs and ultimately lead to organ failure, which is a major cause of disability and death in many diseases. However, the regulatory mechanism of organ fibrosis is not well clear and the lack of effective drugs and treatments, which seriously endangers human health and safety.
View Article and Find Full Text PDFOral and intranasal aspirin desensitisation for non-steroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease.
Cochrane Database Syst Rev
January 2025
Department of Otorhinolaryngology, Amsterdam University Medical Centre, Amsterdam, Netherlands.
Background: NSAID-exacerbated respiratory disease (N-ERD) is a hypersensitivity to non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin or ibuprofen, accompanied by chronic rhinosinusitis (with or without nasal polyps) or asthma. The prevalence of hypersensitivity to NSAIDs is estimated to be 2%. The first line of treatment is the avoidance of NSAIDs.
View Article and Find Full Text PDFProtective Effect of Platycodin D on Allergic Rhinitis in Mice through DPP4/JAK2/STAT3 Pathway Inhibition.
Curr Mol Pharmacol
January 2025
Otolaryngology Department, the Second Hospital of Hebei Medical University, Shijiazhuang, PRChina 050000.
Background: Allergic Rhinitis (AR) is an inflammatory condition characterized by nasal mucosa remodeling, driven by Immunoglobulin E (IgE). Platycodin D (PLD) exhibits a wide range of bioactive properties.
Aim: The aim of this work was to investigate the potential protective effects of PLD on AR, as well as the underlying mechanisms.
Exploring the therapeutic potential of triterpenoid saponins from : Mechanistic insights into hepatoprotection, immunomodulation, anticancer activities, molecular docking, and pharmacokinetics.
Heliyon
December 2024
Department of Botany, Sri Venkateswara University, Tirupati, A.P, 517502, India.
The study comprehensively investigated the therapeutic potential of triterpenoid saponin extract (GST), encompassing its hepatoprotective, immunomodulatory, and anticancer activities. The study employed a Prednisolone (PRD)-induced immunosuppressed rat model to assess the hepatoprotective and immunomodulatory effects of GST. Using this model, GST was found to modulate haematopoiesis, improving RBC, platelet, and WBC counts, underscoring its potential in hematopoietic homeostasis.
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