Exploring the effect of Desmopressin on Bladder Interstitial Cells of Cajal with Detrusor Overactivity

Abstract

Abstract Background: Enuresis is a common pediatric disease in clinical, and the pathogenesis of enuresis is complex and not fully understood. Modern studies have found that enuresis is closely related to detrusor overactivity (DO). Desmopressin (DDAVP) is the most commonly used drug in the clinic for enuresis, but studies have yet to be reported on the direct effects of DDAVP on the Bladder. So this study investigates whether DDAVP can improve DO and explore the underlying mechanism of action. Methods: In this study, the bladder outlet obstruction rat model serum was used to intervene in Bladder interstitial cells of Cajal (ICCs) as a cell model of DO, which dealt with DDAVP-containing serum. ICCs were identified by optical microscope and immunofluorescence. The expression of tyrosine-protein kinase Kit (c-Kit), phosphoinositide 3-kinase (PI3K), protein kinase B (AKT), mechanistic target of rapamycin (mTOR), b-cell lymphoma-2-interacting myosin-like coiled-coil protein (Beclin 1) and microtubule-associated protein one light chain three betas (LC3B) protein levels was detected by Western Blot. Results: The study showed that the expression levels of c-Kit, PI3K, AKT, and mTOR were increased in the model group. DDAVP can effectively inhibit the expression of related proteins. Beclin 1 and LC3B were not significantly changed in the model group while Beclin 1 and LC3B decrased after the DDAVP intervention. Conclusions: DDAVP can improve DO by decreasing c-Kit expression in Bladder ICCs and regulating PI3K/AKT/mTOR signaling pathway, but not acting through autophagy.