Abstract
The antiviral drug Telbivudine (LdT) has an extrahepatic pharmaceutical effect that improves renal inflammation and tubulointerstitial fibrosis. However, the exact mechanism of action requires further investigation. Toll-like receptor 4 (TLR4) is involved in several physiological processes, including inflammation, fibrosis, innate immunity, and hepatitis B virus-associated glomerulonephritis. The epithelial-to-mesenchymal transition (EMT) is the characteristic pathological change in tubulointerstitial fibrosis. In this study, we used transforming growth factor-β (TGF-β) to stimulate human proximal tubular epithelial (HK-2) cells to investigate the effects of LdT in EMT. In addition, we treated HK-2 cells with a TLR4 agonist, lipopolysaccharide, to determine the effect of LdT on TLR4. The results indicated that LdT inhibited the expression of TLR4 and its downstream proteins. It also decreased the release of inflammatory factors, downregulated the TGF-β/Smad signaling pathway, and reversed the EMT changes seen in HK-2 cells. In conclusion, LdT antagonized TLR4 to inhibit EMT in proximal tubular epithelial cells.
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