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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


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.

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