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• W1508851342 abstract "Background and Purpose Type 1 diabetes is a multifactorial inflammatory disease that develops as a result of deregulated immune responses, causing progressive autoimmune destruction of insulin‐producing beta cells of pancreas. 2‐((4‐acetoxyphenyl)‐2‐chloro‐ N ‐methyl) ethylammonium chloride, compound A ( CpdA ), is a selective glucocorticoid receptor ( GR ) agonist that displays strong anti‐inflammatory and immunomodulatory activities. We investigated the therapeutic effectiveness of CpdA in a pharmacological model of type 1 diabetes in mice. Experimental Approach The utility of CpdA in diabetes prevention was evaluated in vivo through its prophylactic administration to male C57BL /6 mice that received multiple low doses of streptozotocin for immunoinflammatory diabetes induction. The effect of CpdA on disease development was studied by measuring blood glucose and insulin level, histopathological examination, determination of the nature of infiltrating cells, pro‐ and anti‐inflammatory cytokine production, and signalling pathways. Key Results Prophylactic in vivo therapy with CpdA conferred protection against development of immunoinflammatory diabetes in mice by dampening the M 1/ T h1/ T h17 immune response and switching it towards an anti‐inflammatory M 2/ T h2/Treg profile, thus preserving beta cell function. Conclusions and Implications Anti‐diabetic properties of CpdA are mediated through modulation of immune cell‐mediated pathways, but without triggering adverse events. These findings provide basic information for the therapeutic use of selective GR agonists in the amelioration of islet‐directed autoimmunity." @default.
• W1508851342 created "2016-06-24" @default.
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• W1508851342 date "2014-11-24" @default.
• W1508851342 modified "2023-09-25" @default.
• W1508851342 title "Compound A, a selective glucocorticoid receptor agonist, inhibits immunoinflammatory diabetes, induced by multiple low doses of streptozotocin in mice" @default.
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• W1508851342 doi "https://doi.org/10.1111/bph.12892" @default.
• W1508851342 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4290725" @default.
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• W1508851342 hasPublicationYear "2014" @default.
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