POSTER ABSTRACTS
Materials should NOT be shared with those that are not registered for the conference. Poster abstracts are not proofed for spelling and/or grammar errors.
The poster and/or other information contained on this website may NOT be downloaded and/or used without prior written permission from all authors on the project. If you would like to be connected with the author(s), please email cme@dmu.edu.
Protective Effects of Empagliflozin Against Experimentally-induced Renal Fibrosis
Sarah Bayne, BS and Shankar Munusamy, MS (Pharm), PhD
College of Pharmacy and Health Sciences, Drake University, Des Moines, IA
Abstract
Background: Chronic kidney disease (CKD) is the condition where the kidneys are unable to filter and clean the blood of waste properly. Fibrosis is regarded as a final common pathway leading to CKD. Our study investigated whether empagliflozin (Jardiance) treatment inhibits transforming growth factor β (TGF-β)-mediated fibrosis and profibrotic signaling in rat renal proximal tubular cells (NRK-52E).
Methods: NRK-52E cells were cultured and treated with TGF-β with or without empagliflozin for 24 and 48 hours. The expression of fibrosis markers - alpha-smooth muscle actin (α-SMA) and vimentin, and TGF--mediated profibrotic signaling - SMAD 2 and 3 - was measured by western blotting.
Results: TGF-β treatment (at 5 ng/mL and 10 ng/mL) induced fibrosis in the kidney cells. Empagliflozin treatment (100 and 500 nM) reduced the expression of the fibrotic markers α-SMA, vimentin, and SMAD-2 and 3 phosphorylation in kidney cells.
Conclusions: Our preliminary findings indicate that TGF-b-mediated induction of fibrosis and profibrotic signaling could be attenuated by empagliflozin treatment. Further studies are required to understand the molecular mechanisms that underpin the antifibrotic effects of empagliflozin against TGF-β-induced renal fibrosis.
Access PDF version to expand view.