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Investigation of the Protective Effects of Dexmedetomidine, Midazolam, Propofol, and Intralipid on Oxidative Stress and Inflammation in Rats with Lidocaine-Induced Toxicity.
J Inflamm Res
January 2025
Department of Anesthesiology, ICU & Perioperative Medicine Hazm Mebaireek General Hospital HMC, Industrial Area Ar-Rayyan, Doha, Qatar.
Aim: The aim of this study was to compare the effects of dexmedetomidine, midazolam, propofol, and intralipid on lidocaine-induced cardiotoxicity and neurotoxicity.
Methods: Forty-eight male Sprague-Dawley rats were randomly divided into six groups (n = 8 per group): control (C), lidocaine (L), lidocaine + dexmedetomidine (LD), lidocaine + midazolam (LM), lidocaine + propofol (LP), and lidocaine + intralipid (LI). Dexmedetomidine (100 µg/kg), midazolam (4 mg/kg), propofol (40 mg/kg), and intralipid (10 mg/kg) were administered intraperitoneally as pretreatment.
Protective Effect of Nerolidol on Paclitaxel-Induced Reproductive Toxicity in Rats: Oxidative Stress and Inflammation.
Basic Clin Pharmacol Toxicol
February 2025
Department of Pharmacology, Faculty of Medicine, Pamukkale University, Denizli, Turkey.
Paclitaxel (PAC), derived from Taxus brevifolia, is used to treat solid tumours but causes reproductive toxicity due to oxidative stress, affecting sperm quality and testicular tissue. Nerolidol (NRL), an antioxidant sesquiterpene alcohol, has not been studied for its potential to reduce PAC-induced reproductive damage. This study investigates NRL's ability to mitigate PAC-induced reproductive toxicity in rats.
View Article and Find Full Text PDFHelminth extracellular vesicles co-opt host monocytes to drive T cell anergy.
J Extracell Vesicles
January 2025
Department of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Parasitic helminths secrete extracellular vesicles (EVs) into their host tissues to modulate immune responses, but the underlying mechanisms are poorly understood. We demonstrate that Ascaris EVs are efficiently internalised by monocytes in human peripheral blood mononuclear cells and increase the percentage of classical monocytes. Furthermore, EV treatment of monocytes induced a novel anti-inflammatory phenotype characterised by CD14, CD16, CC chemokine receptor 2 (CCR2) and programmed death-ligand 1 (PD-L1) cells.
View Article and Find Full Text PDFMicroglial NLRP3-gasdermin D activation impairs blood-brain barrier integrity through interleukin-1β-independent neutrophil chemotaxis upon peripheral inflammation in mice.
Nat Commun
January 2025
Department of Microbiology and Immunology, Brain Korea 21 Project for Medical Science, Institute for Immunology and Immunological Diseases, Yonsei University College of Medicine, Seoul, Republic of Korea.
Blood-brain barrier (BBB) disintegration is a key contributor to neuroinflammation; however, the biological processes governing BBB permeability under physiological conditions remain unclear. Here, we investigate the role of NLRP3 inflammasome in BBB disruption following peripheral inflammatory challenges. Repeated intraperitoneal lipopolysaccharide administration causes NLRP3-dependent BBB permeabilization and myeloid cell infiltration into the brain.
View Article and Find Full Text PDFNonselective beta blockade enhances gut microbiome diversity in a rodent model of trauma, hemorrhage, and chronic stress.
J Trauma Acute Care Surg
November 2024
From the Department of Surgery and Sepsis and Critical Illness Research Center (J.A.M., L.S.K., E.E.P., C.G.A., K.B.K., L.E.B., P.A.E., A.M.M.), University of Florida College of Medicine, Gainesville; and The Gut Biome Lab, Department of Health, Nutrition, and Food Sciences (G.P., R.N.), Florida State University College of Education, Health, and Human Sciences, Tallahassee, Florida.
Background: Traumatic injury leads to gut dysbiosis with changes in microbiome diversity and conversion toward a "pathobiome" signature characterized by a selective overabundance of pathogenic bacteria. The use of non-selective beta antagonism in trauma patients has been established as a useful adjunct to reduce systemic inflammation. We sought to investigate whether beta-adrenergic blockade following trauma would prevent the conversion of microbiome to a "pathobiome" phenotype.
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