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Receptor-interacting protein kinase 3-mediated programmed cell necrosis in rats subjected to focal cerebral ischemia-reperfusion injury

  • Authors:
    • Yanru Dong
    • Cuifen Bao
    • Jingwei Yu
    • Xia Liu
  • View Affiliations / Copyright

    Affiliations: Department of Histology and Embryology, Liaoning Medical University, Jinzhou, Liaoning 121001, P.R. China, Key Laboratory of Molecular Cell Biology and New Drug Development, Liaoning Medical University, Jinzhou, Liaoning 121001, P.R. China
    Copyright: © Dong et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 728-736
    |
    Published online on: May 19, 2016
       https://doi.org/10.3892/mmr.2016.5311
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Abstract

In the current study, the activation of tumor necrosis factor-α receptor 1 (TNFR1) and receptor-interacting protein kinase 3 (RIP3) were investigated following cerebral ischemia-reperfusion injury (CIRI). Healthy SD rats were randomly divided into 3 groups: Sham operation group, model group and inhibitor group. The model group and inhibitor group were further divided into 4 subgroups of 6, 12, 24 and 72 h following CIRI. Using right middle cerebral artery embolization, the CIRI model was generated. To confirm that the CIRI model was established, neurological scores, TTC staining and brain water content measurements were conducted. Immunohistochemistry and western blotting were conducted to investigate the expression of TNFR1 and RIP3 in the cerebral cortex. It was observed that nerve cell necrosis occurred following 6 h of CIRI. The appearance of necrotic cells was gradually increased with increasing CIRI duration. TNFR1 and RIP3 were positively expressed following 6 h of CIRI. With increasing durations of CIRI, the protein expression levels of TNFR1 and RIP3 were significantly increased. Pre‑administration with Z-VAD-FMK (zVAD) significantly increased the protein level of RIP3, however, had no effect on the levels of TNFR1, and was accompanied by a reduction in necrosis. In conclusion, RIP3‑mediated cell necrosis was enhanced by caspase blockade zVAD and the function of zVAD was independent of TNFR1 signaling following IR.
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Copy and paste a formatted citation
Spandidos Publications style
Dong Y, Bao C, Yu J and Liu X: Receptor-interacting protein kinase 3-mediated programmed cell necrosis in rats subjected to focal cerebral ischemia-reperfusion injury. Mol Med Rep 14: 728-736, 2016.
APA
Dong, Y., Bao, C., Yu, J., & Liu, X. (2016). Receptor-interacting protein kinase 3-mediated programmed cell necrosis in rats subjected to focal cerebral ischemia-reperfusion injury. Molecular Medicine Reports, 14, 728-736. https://doi.org/10.3892/mmr.2016.5311
MLA
Dong, Y., Bao, C., Yu, J., Liu, X."Receptor-interacting protein kinase 3-mediated programmed cell necrosis in rats subjected to focal cerebral ischemia-reperfusion injury". Molecular Medicine Reports 14.1 (2016): 728-736.
Chicago
Dong, Y., Bao, C., Yu, J., Liu, X."Receptor-interacting protein kinase 3-mediated programmed cell necrosis in rats subjected to focal cerebral ischemia-reperfusion injury". Molecular Medicine Reports 14, no. 1 (2016): 728-736. https://doi.org/10.3892/mmr.2016.5311
Copy and paste a formatted citation
x
Spandidos Publications style
Dong Y, Bao C, Yu J and Liu X: Receptor-interacting protein kinase 3-mediated programmed cell necrosis in rats subjected to focal cerebral ischemia-reperfusion injury. Mol Med Rep 14: 728-736, 2016.
APA
Dong, Y., Bao, C., Yu, J., & Liu, X. (2016). Receptor-interacting protein kinase 3-mediated programmed cell necrosis in rats subjected to focal cerebral ischemia-reperfusion injury. Molecular Medicine Reports, 14, 728-736. https://doi.org/10.3892/mmr.2016.5311
MLA
Dong, Y., Bao, C., Yu, J., Liu, X."Receptor-interacting protein kinase 3-mediated programmed cell necrosis in rats subjected to focal cerebral ischemia-reperfusion injury". Molecular Medicine Reports 14.1 (2016): 728-736.
Chicago
Dong, Y., Bao, C., Yu, J., Liu, X."Receptor-interacting protein kinase 3-mediated programmed cell necrosis in rats subjected to focal cerebral ischemia-reperfusion injury". Molecular Medicine Reports 14, no. 1 (2016): 728-736. https://doi.org/10.3892/mmr.2016.5311
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