Open Access

Naringin attenuates renal interstitial fibrosis by regulating the TGF‑β/Smad signaling pathway and inflammation

  • Authors:
    • Ruichen Wang
    • Gaolei Wu
    • Tiantian Dai
    • Yitian Lang
    • Zhongchao Chi
    • Shilei Yang
    • Deshi Dong
  • View Affiliations

  • Published online on: November 23, 2020     https://doi.org/10.3892/etm.2020.9498
  • Article Number: 66
  • Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Interstitial fibrosis is a typical feature of all progressive renal diseases. The process of fibrosis is frequently coupled with the presence of pro‑fibrotic factors and inflammation. Naringin is a dihydroflavone compound that has been previously reported to exhibit anti‑fibrotic effects in the liver, where it prevents oxidative damage. In the present study, a rat model of renal interstitial fibrosis and fibrosis cell model were established to evaluate the effects of naringin on inflammatory proteins and fibrosis markers in kidney of rats and NRK‑52E cells, and to elucidate the role of the TGF‑β/Smad signaling pathway in this mechanism. Compared with those in fibrotic NRK‑52E cells that were stimulated by transforming growth factor‑β (TGF‑β), gene expression levels of α‑smooth muscle actin (α‑SMA), collagen 1 (COL1A1), collagen 3 (COL3A1), interleukin (IL)‑1β, IL‑6 and tumor necrosis factor‑α (TNF‑α) were all found to be significantly decreased in fibrotic NRK‑52E cells following treatment with naringin (50, 100 and 200 ng/ml). Results from the histopathological studies showed that naringin treatment preserved the renal tissue structure and reduced the degree of fibrosis in the kidney tissues of rats that underwent unilateral ureteral obstruction (UUO). In addition, naringin administration reduced the expression of α‑SMA, COL1A1, COL3A1, IL‑1β, IL‑6 and TNF‑α in the kidneys of rats following UUO. The current study, using western blot analysis, indicated that naringin also downregulated the activation of Smad2/3 and the expression of Smad4, high‑mobility group protein B1, activator protein‑1, NF‑κB and cyclooxygenase‑2 whilst upregulating the expression of Smad7 in fibrotic NRK‑52E cells and rats in the UUO group. In conclusion, naringin could antagonize renal interstitial fibrosis by regulating the TGF‑β/Smad pathway and the expression of inflammatory factors.
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January-2021
Volume 21 Issue 1

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Copy and paste a formatted citation
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Spandidos Publications style
Wang R, Wu G, Dai T, Lang Y, Chi Z, Yang S and Dong D: Naringin attenuates renal interstitial fibrosis by regulating the TGF‑β/Smad signaling pathway and inflammation. Exp Ther Med 21: 66, 2021
APA
Wang, R., Wu, G., Dai, T., Lang, Y., Chi, Z., Yang, S., & Dong, D. (2021). Naringin attenuates renal interstitial fibrosis by regulating the TGF‑β/Smad signaling pathway and inflammation. Experimental and Therapeutic Medicine, 21, 66. https://doi.org/10.3892/etm.2020.9498
MLA
Wang, R., Wu, G., Dai, T., Lang, Y., Chi, Z., Yang, S., Dong, D."Naringin attenuates renal interstitial fibrosis by regulating the TGF‑β/Smad signaling pathway and inflammation". Experimental and Therapeutic Medicine 21.1 (2021): 66.
Chicago
Wang, R., Wu, G., Dai, T., Lang, Y., Chi, Z., Yang, S., Dong, D."Naringin attenuates renal interstitial fibrosis by regulating the TGF‑β/Smad signaling pathway and inflammation". Experimental and Therapeutic Medicine 21, no. 1 (2021): 66. https://doi.org/10.3892/etm.2020.9498