Hesperetin alleviates renal interstitial fibrosis by inhibiting tubular epithelial‑mesenchymal transition in vivo and in vitro
- Hong‑Wei Wang
- Lei Shi
- Yan‑Ping Xu
- Xing‑Ya Qin
- Qi‑Zhi Wang
Affiliations: Department of Cardiology, People's Hospital of Xianfeng County, Xianfeng, Hubei 445600, P.R. China, Department of Oncology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China, Department of Scientific Research Office, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China, Department of Orthopedics, People's Hospital of Xianfeng County, Xianfeng, Hubei 445600, P.R. China, Department of Gastroenterology, People's Hospital of Xianfeng County, Xianfeng, Hubei 445600, P.R. China
- Published online on: August 18, 2017 https://doi.org/10.3892/etm.2017.4968
Copyright: © Wang
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Hesperetin (HES) is a flavonoid that has been reported to exert protective effects against cardiac remodeling, lung fibrosis and hepatic fibrosis. However, reports on the effects and potential mechanisms of HES in renal fibrosis are limited. In the present study, a unilateral ureteric obstruction (UUO) mouse model and a transforming growth factor (TGF)‑β1‑activated normal rat kidney (NRK)‑52E cell model were established. HES was subsequently administered to these models to evaluate its anti‑fibrotic effects and potential underlying mechanisms of action. The results demonstrated that HES reduced obstruction‑induced renal injury and deposition of the extracellular matrix components collagen‑I and fibronectin in UUO mouse kidneys (P<0.05). Furthermore, HES treatment significantly suppressed EMT, as evidenced by decreased expression of α‑smooth muscle actin and E‑cadherin, (P<0.05). Additionally, HES inhibited the hedgehog signaling pathway in UUO mice and TGF‑β1‑treated NRK‑52E cells. The present findings indicate that HES treatment may inhibit EMT and renal fibrosis in vivo and in vitro by antagonizing the hedgehog signaling pathway.