Objectives: The aim of this study was to investigate changes in disease activity, cytokine profiles, and proliferation of peripheral blood mononuclear cells (PBMCs) in active rheumatoid arthritis (RA) patients treated with simvastatin.
Methods: Thirty-three patients with active RA were prescribed simvastatin (40 mg/day) for 3 months. Most of the patients received background traditional disease-modifying anti-rheumatic drugs (DMARDs) in stable doses. At the end of treatment there was a reduction in the 28-joint Disease Activity Score (DAS28) and in the Health Assessment Questionnaire (HAQ) score.
Results: Eleven patients (33%) achieved a moderate European League Against Rheumatism (EULAR) response. There was a decrease in circulating interleukin (IL)-17 concentrations and spontaneous PBMC proliferation. Anti-CD3-stimulated IL-10 and tumour necrosis factor (TNF)alpha production by PBMCs was upregulated after simvastatin therapy. A reduction in serum IL-6 was detected only in the responder group. Baseline circulating IL-10 concentrations were higher in responders than in non-responders.
Conclusion: Simvastatin treatment is associated with moderate clinical improvement in patients with active RA. Immunological changes produced by simvastatin in peripheral blood are complex and may reflect both its anti- and pro-inflammatory properties.
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http://dx.doi.org/10.1080/03009740802363776 | DOI Listing |
Inflammopharmacology
December 2024
Riphah Institute of Pharmaceutical Sciences, Riphah International University, Lahore Campus, Lahore, 5400, Pakistan.
Rheumatoid arthritis is an autoimmune disorder affecting multiple joints and requires lifelong treatment. Present study was designed to formulate Esculin-loaded chitosan nanoparticles (ENPs) and evaluation of its anti-inflammatory and anti-arthritic action. The acute toxicity study of ENPs was also performed.
View Article and Find Full Text PDFAppl Biochem Biotechnol
December 2024
Department of Biotechnology, Science Campus, Alagappa University, Karaikudi, India.
Early childhood caries (ECC), a severe form of dental caries, is exacerbated by the synergistic interaction between Streptococcus mutans and Candida albicans, leading to greater disease severity than their individual effects. This underscores the need for more targeted and potent therapeutic alternatives. Given the promising anti-infective properties of quaternary ammonium surfactants (QAS), this study explores the microbicidal properties of one such QAS, cetyltrimethylammonium chloride (CTAC), against both individual- and dual-species cultures of S.
View Article and Find Full Text PDFMol Neurobiol
December 2024
Department of Neurology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Virus encephalitis (VE), recognized as one of the common kinds of central nervous system (CNS) diseases after virus infection, has a surprising correlation with autoimmune encephalitis (AE) when autoimmune antibodies emerge in cerebrospinal fluid (CSF) or serum. Herpes simplex virus and Epstein-Barr virus are the most critical agents worldwide. By molecular mimicry, herpes viruses can invade the brain directly or indirectly.
View Article and Find Full Text PDFCurr Rheumatol Rep
December 2024
Department of Medicine, Division of Rheumatology, Queen's University, Kingston, ON, Canada.
Purpose Of Review: The canonical pathogenesis of spondyloarthritis (SpA) involves inflammation driven by HLA-B27, type 3 immunity, and gut microbial dysregulation. This review based on information presented at the SPARTAN meeting highlights studies on the pathogenesis of SpA from the past year, focusing on emerging mechanisms such as the roles of microbe-derived metabolites, microRNAs (miRNAs) and cytokines in plasma exosomes, specific T cell subsets, and neutrophils.
Recent Findings: The induction of arthritis in a preclinical model through microbiota-driven alterations in tryptophan catabolism provides new insights as to how intestinal dysbiosis may activate disease via the gut-joint axis.
Protein Sci
January 2025
Department of Neuroscience, Biomedicine and Movement Sciences, Section of Biochemistry, University of Verona, Verona, Italy.
Human succinic semialdehyde dehydrogenase is a mitochondrial enzyme fundamental in the neurotransmitter γ-aminobutyric acid catabolism. It catalyzes the NAD-dependent oxidative degradation of its derivative, succinic semialdehyde, to succinic acid. Mutations in its gene lead to an inherited neurometabolic rare disease, succinic semialdehyde dehydrogenase deficiency, characterized by mental and developmental delay.
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