Tadalafil, a PDE5 inhibitor, Exhibits Renoprotective Effects Preventing Podocyte Damage in an Adriamycin-Induced Nephrotic Syndrome Model
Abstract
Background: Phosphodiesterase (PDE)-5 inhibitor is reportedly a renoprotective compound. Although PDE5 expression is confirmed in the glomeruli, its relationship with renal dysfunction remains elusive. We have previously investigated the renoprotective effects of tadalafil in a CKD model (Tomita N, et al. Physiol Rep. 2020), suggesting that such an effect would be related to podocyte damage attenuation. In this study, we investigated how tadalafil, a PDE5 inhibitor, could affect a rat nephrotic syndrome model. Methods: Wistar ST rats were established as nephrotic syndrome models by administrating adriamycin (ADR) injection. The animals were divided into 3 groups: control (n = 6), ADR (n = 5), and ADR + tadalafil (n = 5). Tadalafil was administered 10 mg/kg daily. After 2 weeks of treatment, the urinary protein and serum albumin levels were evaluated, and the kidney tissue was harvested. WT1-positive cells were identified as podocytes by WT1 immunostaining. Moreover, human renal glomerular epithelial cell damage was induced in vitro by ADR supplementation. After 24 h of ADR treatment with or without tadalafil, cell viability was determined using CCK-8. Results: The ADR injection induced high urinary protein and low serum albumin levels. Two weeks of tadalafil treatment attenuated proteinuria compared to the ADR group (P<0.01). ADR reduced the WT1-positive cell number and the tadalafil treatment prevented the reduction (P<0.05). Moreover, the ADR treatment resulted in reduced…
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