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- W2396998519 abstract "Type 1 diabetes in mice is characterized by autoimmune destruction of insulin-producing pancreatic β-cells. Disease pathogenesis involves invasion of pancreatic islets by immune cells, including macrophages and T cells, and production of antibodies to self-antigens, including insulin. Activation of the inflammatory reflex, the neural circuit that inhibits inflammation, culminates on cholinergic receptor signals on immune cells to attenuate cytokine release and inhibit B-cell antibody production. Here, we show that galantamine, a centrally acting acetylcholinesterase inhibitor and an activator of the inflammatory reflex, attenuates murine experimental type 1 diabetes. Administration of galantamine to animals immunized with keyhole limpet hemocyanin (KLH) significantly suppressed splenocyte release of immunoglobulin G (IgG) and interleukin (IL)-4 and IL-6 during KLH challenge ex vivo. Administration of galantamine beginning at 1 month of age in nonobese diabetic (NOD) mice significantly delayed the onset of hyperglycemia, attenuated immune cell infiltration in pancreatic islets and decreased anti-insulin antibodies in serum. These observations indicate that galantamine attenuates experimental type 1 diabetes in mice and suggest that activation of the inflammatory reflex should be further studied as a potential therapeutic approach." @default.
- W2396998519 created "2016-06-24" @default.
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- W2396998519 creator A5075492017 @default.
- W2396998519 date "2015-01-01" @default.
- W2396998519 modified "2023-10-14" @default.
- W2396998519 title "Galantamine Attenuates Type 1 Diabetes and Inhibits Anti-Insulin Antibodies in Nonobese Diabetic Mice" @default.
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- W2396998519 doi "https://doi.org/10.2119/molmed.2015.00142" @default.
- W2396998519 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4749496" @default.
- W2396998519 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26322849" @default.
- W2396998519 hasPublicationYear "2015" @default.
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