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Influence of melatonin on IL-1Ra gene and IL-1 expression in rats with liver ischemia reperfusion injury

  • Authors:
    • Hong Zhou
    • Chunhui Jiang
    • Lei Gu
    • Ye Liu
    • Longci Sun
    • Qing Xu
  • View Affiliations / Copyright

    Affiliations: Department of Gastrointestinal Surgery, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, P.R. China
    Copyright: © Zhou et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 667-672
    |
    Published online on: April 4, 2016
       https://doi.org/10.3892/br.2016.645
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Abstract

The aim of the present study was to explore the influence of melatonin (MT) on rats with liver ischemia reperfusion injury (IRI) and its mechanism. A total of 66 male Sprague‑Dawley rats were randomly divided into 3 groups: i) Normal control group, ii) ischemia reperfusion group (IR group) and iii) melatonin treatment group (MT group). Rats in the MT group were administered an intraperitoneal injection of MT (10 mg/kg, 1 ml) at 70 and 35 min before ischemia, early reperfusion, and 1 and 2 h after reperfusion, respectively. Blood was removed at the normal time-point (prior to any processes), 35 min before ischemia, 2, 4, 8 and 24 h after reperfusion. Subsequently the rats were sacrificed. The pathological changes of liver tissues, interleukin-1 receptor antagonist (IL-1Ra) gene and IL-1 expression levels were detected. There were no evident differences between the immediate reperfusion and 2 h IR group and MT group. The liver structure injury of the 4, 8 and 24 h MT groups were improved to various differences compared to the corresponding IR group; liver IL-1β of the MT group at 35 min after ischemia, and 2, 4, 8 and 24 h after reperfusion was evidently lower than that of the IR group (P<0.05); IL-1Ra mRNA expression in the 2 h MT group was higher compared to the 2 h IR group by 4.85-fold; and IL-1Ra mRNA expression in the 4 h MT group was higher compared to the 4 h IR group by 9.34-fold. Differences between two groups at other time-points were <2-fold. In conclusion, MT can upregulate IL-1Ra gene expression by reducing generation of IL-1 thus reducing IRI.
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Copy and paste a formatted citation
Spandidos Publications style
Zhou H, Jiang C, Gu L, Liu Y, Sun L and Xu Q: Influence of melatonin on IL-1Ra gene and IL-1 expression in rats with liver ischemia reperfusion injury. Biomed Rep 4: 667-672, 2016.
APA
Zhou, H., Jiang, C., Gu, L., Liu, Y., Sun, L., & Xu, Q. (2016). Influence of melatonin on IL-1Ra gene and IL-1 expression in rats with liver ischemia reperfusion injury. Biomedical Reports, 4, 667-672. https://doi.org/10.3892/br.2016.645
MLA
Zhou, H., Jiang, C., Gu, L., Liu, Y., Sun, L., Xu, Q."Influence of melatonin on IL-1Ra gene and IL-1 expression in rats with liver ischemia reperfusion injury". Biomedical Reports 4.6 (2016): 667-672.
Chicago
Zhou, H., Jiang, C., Gu, L., Liu, Y., Sun, L., Xu, Q."Influence of melatonin on IL-1Ra gene and IL-1 expression in rats with liver ischemia reperfusion injury". Biomedical Reports 4, no. 6 (2016): 667-672. https://doi.org/10.3892/br.2016.645
Copy and paste a formatted citation
x
Spandidos Publications style
Zhou H, Jiang C, Gu L, Liu Y, Sun L and Xu Q: Influence of melatonin on IL-1Ra gene and IL-1 expression in rats with liver ischemia reperfusion injury. Biomed Rep 4: 667-672, 2016.
APA
Zhou, H., Jiang, C., Gu, L., Liu, Y., Sun, L., & Xu, Q. (2016). Influence of melatonin on IL-1Ra gene and IL-1 expression in rats with liver ischemia reperfusion injury. Biomedical Reports, 4, 667-672. https://doi.org/10.3892/br.2016.645
MLA
Zhou, H., Jiang, C., Gu, L., Liu, Y., Sun, L., Xu, Q."Influence of melatonin on IL-1Ra gene and IL-1 expression in rats with liver ischemia reperfusion injury". Biomedical Reports 4.6 (2016): 667-672.
Chicago
Zhou, H., Jiang, C., Gu, L., Liu, Y., Sun, L., Xu, Q."Influence of melatonin on IL-1Ra gene and IL-1 expression in rats with liver ischemia reperfusion injury". Biomedical Reports 4, no. 6 (2016): 667-672. https://doi.org/10.3892/br.2016.645
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