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• W3021551569 abstract "INTRODUCTION AND OBJECTIVE: Due in large part to damaging changes caused by inflammation during bladder outlet obstruction, bladder dysfunction persists in many patients following de-obstruction surgery. Our lab has extensively studied the mechanisms that trigger the inflammatory response, but the role of endogenous anti-inflammatories in the bladder, notably Annexin A1, has never been explored. In this study we tested the ability of Annexin A1 to expedite the resolution of inflammation following de-obstruction and improve bladder function recovery. METHODS: Sprague Dawley rats underwent bladder outlet obstruction via urethral ligation around a 1 mm (o.d.) catheter. De-obstruction was performed after 12 days and rats were randomized to treatment with 1 mg/kg/day of AC2-26 (the active N-terminal peptide of Annexin A1) in PBS or vehicle for two days. For inflammation assays, 25 mg/kg of Evans blue dye was injected IV one hour prior to sacrifice. Bladders were then weighed and Evans blue concentrations measured spectrophotometrically. For functional assays, suprapubic tubes were placed at the time of obstruction and cystometry performed two days after de-obstruction. Functional assays included a sham surgery group while inflammation assays included a no-treatment group to establish controls. The sham cohort underwent loose urethral ligature placement and subsequent removal after 12 days. RESULTS: Bladder weights increased from 289.9 mg after 12 days of obstruction to 336.0 mg two days after de-obstruction while treatment with AC2-26 reduced this to 252.0 mg. Inflammation measured by Evans blue extravasation decreased following de-obstruction from 27.8 ng EB/mg to 21.88 ng EB/mg after two days; AC2-26 further decreased this to 15.5 ng EB/mg which was significantly different from the obstructed baseline. Functionally, 83% of rats that received AC2-26 had a return of normal micturition after 2 days as compared to 50% who received vehicle only and 100% of sham operated rats. CONCLUSIONS: We demonstrated that the resolution of inflammation following de-obstruction is augmented significantly when treated with AC2-26. Furthermore, the addition of AC2-26 results in improved return of micturition cycles even when controlled for the effects of surgery. Overall these results demonstrate that Annexin A1 can enhance the resolution of inflammation following bladder de-obstruction and this correlates with improved bladder function. Source of Funding: National Institute of Diabetes and Digestive and Kidney Diseases (DK103534 to J.T.P.) and intramural funds from Duke University" @default.
• W3021551569 created "2020-05-13" @default.
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• W3021551569 date "2020-04-01" @default.
• W3021551569 modified "2023-10-17" @default.
• W3021551569 title "MP28-03 THE ENDOGENOUS ANTI-INFLAMMATORY ANNEXIN A1 AUGMENTS RECOVERY FOLLOWING BLADDER OUTLET DE-OBSTRUCTION" @default.
• W3021551569 doi "https://doi.org/10.1097/ju.0000000000000867.03" @default.
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