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Article Open Access

Sinomenine alleviates dextran sulfate sodium‑induced colitis via the Nrf2/NQO‑1 signaling pathway

  • Authors:
    • Yan Zhou
    • Hanyang Liu
    • Jun Song
    • Liang Cao
    • Liming Tang
    • Chunjian Qi
  • View Affiliations / Copyright

    Affiliations: Medical Research Center, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, Jiangsu 213003, P.R. China, Department of Gastrointestinal Surgery, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, Jiangsu 213003, P.R. China
    Copyright: © Zhou et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 4.0].
  • Pages: 3691-3698
    |
    Published online on: August 10, 2018
       https://doi.org/10.3892/mmr.2018.9378
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Abstract

Sinomenine (SIN), a pure alkaloid isolated from Sinomenium acutum, has been widely used in arthritis for its anti‑inflammatory effect, but little is known about the effect of SIN on human ulcerative colitis (UC). In the present study, the effect and mechanism of SIN was examined in a dextran sulfate sodium (DSS)‑induced murine colitis model, which mimics human UC. Oral administration of SIN significantly suppressed the elevated disease activity index and ameliorated colonic histological damage in a DSS‑induced colitis model. Tumor necrosis factor‑α, interleukin‑6 and inducible nitric oxide synthase levels were also reduced as detected by reverse transcription‑quantitative polymerase chain reaction. In addition, SIN reversed the decreased colon length and colonic superoxide dismutase activity. Furthermore, western blot analysis revealed that nuclear factor‑erythroid 2‑related factor 2 (Nrf2) and its downstream genes, heme oxygenase‑1 and NADP(H) quinone oxidoreductase 1 (NQO‑1), were markedly activated by SIN. The current results indicated that SIN alleviated DSS‑induced colitis in mice, which may be due to its antioxidant properties and was at least in part dependent on the Nrf2/NQO‑1 signaling pathway. Therefore, SIN may have potential applications as a protective drug for patients with UC.
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Copy and paste a formatted citation
Spandidos Publications style
Zhou Y, Liu H, Song J, Cao L, Tang L and Qi C: Sinomenine alleviates dextran sulfate sodium‑induced colitis via the Nrf2/NQO‑1 signaling pathway. Mol Med Rep 18: 3691-3698, 2018.
APA
Zhou, Y., Liu, H., Song, J., Cao, L., Tang, L., & Qi, C. (2018). Sinomenine alleviates dextran sulfate sodium‑induced colitis via the Nrf2/NQO‑1 signaling pathway. Molecular Medicine Reports, 18, 3691-3698. https://doi.org/10.3892/mmr.2018.9378
MLA
Zhou, Y., Liu, H., Song, J., Cao, L., Tang, L., Qi, C."Sinomenine alleviates dextran sulfate sodium‑induced colitis via the Nrf2/NQO‑1 signaling pathway". Molecular Medicine Reports 18.4 (2018): 3691-3698.
Chicago
Zhou, Y., Liu, H., Song, J., Cao, L., Tang, L., Qi, C."Sinomenine alleviates dextran sulfate sodium‑induced colitis via the Nrf2/NQO‑1 signaling pathway". Molecular Medicine Reports 18, no. 4 (2018): 3691-3698. https://doi.org/10.3892/mmr.2018.9378
Copy and paste a formatted citation
x
Spandidos Publications style
Zhou Y, Liu H, Song J, Cao L, Tang L and Qi C: Sinomenine alleviates dextran sulfate sodium‑induced colitis via the Nrf2/NQO‑1 signaling pathway. Mol Med Rep 18: 3691-3698, 2018.
APA
Zhou, Y., Liu, H., Song, J., Cao, L., Tang, L., & Qi, C. (2018). Sinomenine alleviates dextran sulfate sodium‑induced colitis via the Nrf2/NQO‑1 signaling pathway. Molecular Medicine Reports, 18, 3691-3698. https://doi.org/10.3892/mmr.2018.9378
MLA
Zhou, Y., Liu, H., Song, J., Cao, L., Tang, L., Qi, C."Sinomenine alleviates dextran sulfate sodium‑induced colitis via the Nrf2/NQO‑1 signaling pathway". Molecular Medicine Reports 18.4 (2018): 3691-3698.
Chicago
Zhou, Y., Liu, H., Song, J., Cao, L., Tang, L., Qi, C."Sinomenine alleviates dextran sulfate sodium‑induced colitis via the Nrf2/NQO‑1 signaling pathway". Molecular Medicine Reports 18, no. 4 (2018): 3691-3698. https://doi.org/10.3892/mmr.2018.9378
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