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Effects and mechanisms of CTRP3 overexpression in secondary brain injury following intracerebral hemorrhage in rats

  • Authors:
    • Yu Wan
    • Jieqiong Wang
    • Bo Yang
    • Conggai Huang
    • Xiaoqin Tang
    • Hong Yi
    • Yun Liu
    • Shaohua Wang
  • View Affiliations / Copyright

    Affiliations: Department of Pathology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuang 646000, P.R. China
    Copyright: © Wan et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 35
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    Published online on: November 9, 2021
       https://doi.org/10.3892/etm.2021.10957
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Abstract

C1q/TNF‑related protein‑3 (CTRP3) is a novel adipokine that serves an important role in oxidative stress, anti‑apoptosis, anti‑inflammation and immune regulation. The aim of the present study was to investigate the protective role of CTRP3 against intracerebral hemorrhage (ICH)‑induced brain injury. A model of autologous arterial blood‑induced ICH was constructed in rats. Intracerebral infusion of a lentivirus carrying the CTRP3 gene was used to induce CTRP3 overexpression in the brain. The effects and mechanisms of CTRP3 overexpression on brain injury were investigated by detecting brain edema, blood‑brain barrier (BBB) integrity, neurological function and inflammatory‑associated factors 3 days after ICH. The present results demonstrated that CTRP3 overexpression ameliorated ICH‑induced neurological dysfunction, decreased brain edema, maintained BBB integrity and attenuated inflammation. The protective effect of CTRP3 overexpression was associated with increased activation of silent information regulator 1 (SIRT1). In conclusion, the present study demonstrated that CTRP3 overexpression protected against ICH‑induced brain injury in rats, potentially via activating the SIRT1 signaling pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Wan Y, Wang J, Yang B, Huang C, Tang X, Yi H, Liu Y and Wang S: Effects and mechanisms of CTRP3 overexpression in secondary brain injury following intracerebral hemorrhage in rats. Exp Ther Med 23: 35, 2022.
APA
Wan, Y., Wang, J., Yang, B., Huang, C., Tang, X., Yi, H. ... Wang, S. (2022). Effects and mechanisms of CTRP3 overexpression in secondary brain injury following intracerebral hemorrhage in rats. Experimental and Therapeutic Medicine, 23, 35. https://doi.org/10.3892/etm.2021.10957
MLA
Wan, Y., Wang, J., Yang, B., Huang, C., Tang, X., Yi, H., Liu, Y., Wang, S."Effects and mechanisms of CTRP3 overexpression in secondary brain injury following intracerebral hemorrhage in rats". Experimental and Therapeutic Medicine 23.1 (2022): 35.
Chicago
Wan, Y., Wang, J., Yang, B., Huang, C., Tang, X., Yi, H., Liu, Y., Wang, S."Effects and mechanisms of CTRP3 overexpression in secondary brain injury following intracerebral hemorrhage in rats". Experimental and Therapeutic Medicine 23, no. 1 (2022): 35. https://doi.org/10.3892/etm.2021.10957
Copy and paste a formatted citation
x
Spandidos Publications style
Wan Y, Wang J, Yang B, Huang C, Tang X, Yi H, Liu Y and Wang S: Effects and mechanisms of CTRP3 overexpression in secondary brain injury following intracerebral hemorrhage in rats. Exp Ther Med 23: 35, 2022.
APA
Wan, Y., Wang, J., Yang, B., Huang, C., Tang, X., Yi, H. ... Wang, S. (2022). Effects and mechanisms of CTRP3 overexpression in secondary brain injury following intracerebral hemorrhage in rats. Experimental and Therapeutic Medicine, 23, 35. https://doi.org/10.3892/etm.2021.10957
MLA
Wan, Y., Wang, J., Yang, B., Huang, C., Tang, X., Yi, H., Liu, Y., Wang, S."Effects and mechanisms of CTRP3 overexpression in secondary brain injury following intracerebral hemorrhage in rats". Experimental and Therapeutic Medicine 23.1 (2022): 35.
Chicago
Wan, Y., Wang, J., Yang, B., Huang, C., Tang, X., Yi, H., Liu, Y., Wang, S."Effects and mechanisms of CTRP3 overexpression in secondary brain injury following intracerebral hemorrhage in rats". Experimental and Therapeutic Medicine 23, no. 1 (2022): 35. https://doi.org/10.3892/etm.2021.10957
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