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Fisetin inhibits pristine-induced systemic lupus erythematosus in a murine model through CXCLs regulation

  • Authors:
    • Su‑Ping Xu
    • Yong‑Sheng Li
  • View Affiliations / Copyright

    Affiliations: Department of Dermatology, Affiliated Huai'an No. 1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu 223300, P.R. China, Department of Rheumatology, Affiliated Huai'an No. 1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu 223300, P.R. China
    Copyright: © Xu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 3220-3230
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    Published online on: October 1, 2018
       https://doi.org/10.3892/ijmm.2018.3903
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Abstract

Systemic lupus erythematosus (SLE) is associated with an increased risk of vascular complications. Lupus nephritis is a major manifestation of SLE in the clinic. Lupus nephritis is elevated by T helper type 17 (Th17) cells, the major pro‑inflammatory T‑cell subset, leading to autoimmunity modulation. Therapeutic treatments targeting leukocyte recruitment may be useful in attenuating vascular complications linked to SLE progression. 3,7,3',4'‑Tetrahydroxyflavone (fisetin) is a flavonol and a member of the flavonoid polyphenols. It is present in various fruits and vegetables, including persimmons, apples, kiwis, grapes, onions, strawberries and cucumbers. In the present study, the effects of fisetin against SLE induced by pristane (PRI) were evaluated in mice. Fisetin was indicated to reduce PRI‑induced anti‑double stranded DNA, anti‑ small nuclear ribonucleoprotein and the ratio of albumin to creatinine in urine. In addition, the chemokine (C‑X‑C motif) ligand (CXCL) signaling pathway was activated for PRI treatment, which was reversed by fisetin administration by reducing CXCL‑1 and 2, chemokine (C‑C motif) ligand 3, as well as CXC receptor 2 expression. In addition, the induction of inflammatory cytokines, including interleukin (IL)‑6, tumor necrosis factor‑α, IL‑1β, as well as the chemokine interferon‑γ, by PRI were downregulated by fisetin treatment in mice. Furthermore, Th17 cells and their associated cytokines were highly induced by PRI treatment, which was inhibited by fisetin administration. The present results indicated that fisetin may be an effective management for SLE by targeting the CXCL signaling pathway and regulating Th17 differentiation during lupus nephritis development.
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Copy and paste a formatted citation
Spandidos Publications style
Xu SP and Li YS: Fisetin inhibits pristine-induced systemic lupus erythematosus in a murine model through CXCLs regulation. Int J Mol Med 42: 3220-3230, 2018.
APA
Xu, S., & Li, Y. (2018). Fisetin inhibits pristine-induced systemic lupus erythematosus in a murine model through CXCLs regulation. International Journal of Molecular Medicine, 42, 3220-3230. https://doi.org/10.3892/ijmm.2018.3903
MLA
Xu, S., Li, Y."Fisetin inhibits pristine-induced systemic lupus erythematosus in a murine model through CXCLs regulation". International Journal of Molecular Medicine 42.6 (2018): 3220-3230.
Chicago
Xu, S., Li, Y."Fisetin inhibits pristine-induced systemic lupus erythematosus in a murine model through CXCLs regulation". International Journal of Molecular Medicine 42, no. 6 (2018): 3220-3230. https://doi.org/10.3892/ijmm.2018.3903
Copy and paste a formatted citation
x
Spandidos Publications style
Xu SP and Li YS: Fisetin inhibits pristine-induced systemic lupus erythematosus in a murine model through CXCLs regulation. Int J Mol Med 42: 3220-3230, 2018.
APA
Xu, S., & Li, Y. (2018). Fisetin inhibits pristine-induced systemic lupus erythematosus in a murine model through CXCLs regulation. International Journal of Molecular Medicine, 42, 3220-3230. https://doi.org/10.3892/ijmm.2018.3903
MLA
Xu, S., Li, Y."Fisetin inhibits pristine-induced systemic lupus erythematosus in a murine model through CXCLs regulation". International Journal of Molecular Medicine 42.6 (2018): 3220-3230.
Chicago
Xu, S., Li, Y."Fisetin inhibits pristine-induced systemic lupus erythematosus in a murine model through CXCLs regulation". International Journal of Molecular Medicine 42, no. 6 (2018): 3220-3230. https://doi.org/10.3892/ijmm.2018.3903
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