Resolvin D1 (RvD1) and its aspirin-triggered epimeric form\n(AT-RvD1) are endogenous lipid mediators (derived from\ndocosahexaenoic acid, DHA) that control the duration and\nmagnitude of inflammation in models of complex diseases. Our\nprevious studies demonstrated that RvD1-mediated signaling\npathways are expressed and active in salivary glands from rodents\nand humans. Furthermore, treatment of salivary cells with RvD1\nblocked TNF-�±-mediated inflammatory signals and improved\nepithelial integrity. The purpose of this pilot study was to determine\nthe feasibility of treatment with AT-RvD1 versus dexamethasone\n(DEX) on inflammation (i.e., lymphocytic infiltration, cytokine\nexpression and apoptosis) observed in submandibular glands\n(SMG) from the NOD/ShiLtJ Sj�¶grenâ��s syndrome (SS) mouse\nmodel before experimenting with a larger population. NOD/ShiLtJ\nmice were treated intravenously with NaCl (0.9%, negative control),\nAT-RvD1 (0.01-0.1 mg/kg) or DEX (4.125-8.25 mg/kg) twice a\nweek for 14 weeks beginning at 4 weeks of age. At 18 weeks of\nage, SMG were collected for pathological analysis and detection of\nSS-associated inflammatory genes. The AT-RvD1 treatment alone\ndid not affect lymphocytic infiltration seen in NOD/ShiLtJ mice\nwhile DEX partially prevented lymphocytic infiltration. Interestingly,\nboth AT-RvD1 and DEX caused downregulation of SS-associated\ninflammatory genes and reduction of apoptosis. Results from this\npilot study suggest that a systemic treatment with AT-RvD1 and\nDEX alone attenuated inflammatory responses observed in the\nNOD/ShiLtJ mice; therefore, they may be considered as potential\ntherapeutic tools in treating SS patients when used alone or in\ncombination
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