Introduction: Multiple sclerosis (MS), as a destructive pathology of myelin in central nervous system (CNS), causes physical and mental complications. Experimental autoimmune encephalomyelitis (EAE) is laboratory model of MS widely used for CNS-associated inflammatory researches. Cell therapy using macrophage M2 (MPM2) is a cell type with anti-inflammatory characteristics for all inflammatory-based neuropathies. This experimental study investigated the probable therapeutic anti-inflammatory effects of intraperitoneal (IP) injection of MPM2 on alleviation of motor defect in EAE-affected animals.
Materials And Methods: 24 C57/BL6 female mice were divided into four groups of EAE, EAE + Dexa, EAE + PBS, and EAE + MP2. EAE was induced through deep cervical injection of spinal homogenate of guinea pigs. MPM2 cells were harvested from bone marrow and injected (10cells/ml) in three days of 10, 13 and 16 post-immunizations (p.i). Clinical score (CS), anti-inflammatory cytokines (IL-4, IL-10), pro-inflammatory gene expression (TNF-α, IL-1β) and histopathological investigations (HE, Nissl and Luxol Fast Blue) were considered. Data were analyzed using SPSS software (v.19) and p < 0.05 was considered significant level.
Results: During EAE induction, the mean animal weight was decreased (p < 0.05); besides, following MPM2 injection, the weight gain was applied (p < 0.05) in EAE + MPM2 groups than control. Increased (p < 0.05) levels of CS was found during EAE induction in days 17-28 in EAE animals; besides, CS was decreased (p < 0.05) in EAE + MPM2 group than EAE animals. Also, in days 25-28 of experiment, the CS was decreased (p < 0.05) in EAE + MPM2 than EAE + Dexa. Histopathological assessments revealed low density of cell nuclei in corpus callosum, microscopically. LFB staining also showed considerable decrease in white matter density of corpus callosum in EAE group. Acceleration of white matter density was found in EAE + MPM2 group following cell therapy procedure. Genes expression of TNF-α, IL-1β along with IL-4 and IL-10 were decreased (p < 0.05) in EAE + MPM2 group.
Conclusion: IP injection of MPM2 to EAE-affected female mice can potentially reduce the CNS inflammation, neuronal death and myelin destruction. MPM2 cell therapy can improve animal motor defects.
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http://dx.doi.org/10.1016/j.trim.2024.102067 | DOI Listing |
Allergol Immunopathol (Madr)
January 2025
Department of Pediatrics, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zheiiang, China.
To illustrate the potential of mesenchymal stem cell-derived exosomes (MSC-Exos) in mitigating septic lung injury by reducing the excessive formation of neutrophil extracellular traps (NETs), a mouse model of septic lung injury was induced through cecal ligation and puncture (CLP). The mice received intraperitoneal injections of MSC-Exos. Post injection, pathological alterations of the lung tissue were evaluated through HE staining, and the levels of inflammatory markers in each mouse group at various time points were assessed using ELISA kits.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Illinois College of Medicine at Peoria, Peoria, IL, USA.
Background: Many lines of evidence support that systemic inflammation promotes Alzheimer's disease (AD) progression. Amyloid plaques are closely accompanied with neuroinflammation characterized by activated microglia and reactive astrocytes. Aging is the largest known risk factor for AD and is characterized by chronic, systemic, low-grade inflammation (inflamm-aging).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
USC Leonard Davis School of Gerontology, Los Angeles, CA, USA.
Background: Iron is implicated in Alzheimer's disease (AD) and is bound to β-amyloid (Ab) plaques. AD brains have increased 4-hydroxynonenal (HNE) adducts, a lipid decomposition product bound to proteins originating from iron mediated lipid peroxidation. Increased brain iron may result from cerebral microbleeds which by nature are rich sources of iron.
View Article and Find Full Text PDFBackground: Senile dementia (SD) is a deteriorative organic brain disorder and it comprises Alzheimer's disease (AD) as a major variant. SD is shown impairment of mental capacities whereas AD is degeneration of neurons. According to World Health Organization (WHO) report; more than 55 million peoples have dementia and it is raising 10 million new cases every year.
View Article and Find Full Text PDFBackground: Alzheimer's disease (AD) is a progressive neurodegenerative disease associated with neuroinflammation and heightened production of reactive oxygen species (ROS) in the brain from overactive NADPH Oxidase 2 (NOX2). The current study examines whether administration of a novel, brain-penetrant NOX2 inhibitor (CPP11G & CPP11H) reduces amyloid plaque load and improves AD-associated vascular dysfunction in a male APP-PS1 mouse model of AD.
Method: Intraperitoneal injections of CPP11G (n = 1) or CPP11H (n = 2) three times per week began at 9-10 months of age in the treatment APP-PS1 group (15 mg/kg).
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