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The protective effects of melatonin postconditioning in cerebral ischemia may be mediated through the modulation of FUNDC1 and Bnip3 levels.

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Title: The protective effects of melatonin postconditioning in cerebral ischemia may be mediated through the modulation of FUNDC1 and Bnip3 levels.
Authors: Aslan, Gulnur (AUTHOR), Bulmus, Ozgur (AUTHOR), Tuzcu, Mehmet (AUTHOR), Gokdere, Ebru (AUTHOR), Can Sahna, Kezban (AUTHOR), Sahin, Kazim (AUTHOR), Sahna, Engin (AUTHOR)
Source: Brain Injury. 2026, Vol. 40 Issue 7, p603-613. 11p.
Subjects: Adipokines, Age of onset, Autophagy, Reperfusion injury, Ischemia, Research funding, Data analysis, MicroRNA, Polymerase chain reaction, Enzyme-linked immunosorbent assay, Parameters (Statistics), Melatonin, Cellular signal transduction, Descriptive statistics, Mitochondrial proteins, Rats, Experimental design, Cerebral cortex, Mathematical statistics, Animal experimentation, Cardiovascular surgery, One-way analysis of variance, Statistics, Neuropsychological tests, Western immunoblotting, Cerebral ischemia, Cell survival, Membrane proteins, Biomarkers
Geographic Terms: Turkey
Abstract: Objective: The regulation of mitochondrial bioenergetics – as one of the endogenous defense mechanisms against ischemia-reperfusion (IR) injury – has been considered promising. This study aimed to determine which mitophagy-related signaling pathways (parkin, Bnip3, or FUNDC1) mediate the protective effects of postconditioning (PostC) and melatonin, both of which enhance the intrinsic defense capacity of cerebral tissue. In addition, microRNA-137 and microRNA-145, as well as serum asprosin, a novel glucogenic adipokine, levels were analyzed in cerebral IR injury. Method: Rats were divided into four groups: control (sham), IR, IR+PostC and IR+Mel(n:10). After 90 minutes of occlusion, PostC was performed at the onset of reperfusion in three cycles of 30-sec reperfusion, followed by 10-sec ischemia. Results: All parameters involved in mitophagy pathways increased with IR in cerebral cortex, and serum asprosin level decreased. Parkin and PINK1 levels did not change due to the treatments, while the FUNDC1 and Bnip3 levels decreased and serum asprosin levels increased significantly compared to IR. MicroRNA-137 and microRNA-145 decreased, although treatment partially restored the levels of these microRNAs. Conclusion: Increased expressions of parkin/PINK1, FUNDC1 and Bnip3 may suggest that all mitophagy pathways are activated by cerebral IR. Melatonin PostC may protect the cerebral tissue by inhibiting BNİP3- and FUNDC1-mediated mitophagy. [ABSTRACT FROM AUTHOR]
Copyright of Brain Injury is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: The protective effects of melatonin postconditioning in cerebral ischemia may be mediated through the modulation of FUNDC1 and Bnip3 levels.
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  Data: <searchLink fieldCode="AR" term="%22Aslan%2C+Gulnur%22">Aslan, Gulnur</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Bulmus%2C+Ozgur%22">Bulmus, Ozgur</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Tuzcu%2C+Mehmet%22">Tuzcu, Mehmet</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Gokdere%2C+Ebru%22">Gokdere, Ebru</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Can+Sahna%2C+Kezban%22">Can Sahna, Kezban</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Sahin%2C+Kazim%22">Sahin, Kazim</searchLink> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Sahna%2C+Engin%22">Sahna, Engin</searchLink> (AUTHOR)
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  Data: <searchLink fieldCode="JN" term="%22Brain+Injury%22">Brain Injury</searchLink>. 2026, Vol. 40 Issue 7, p603-613. 11p.
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  Data: <searchLink fieldCode="DE" term="%22Turkey%22">Turkey</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Objective: The regulation of mitochondrial bioenergetics – as one of the endogenous defense mechanisms against ischemia-reperfusion (IR) injury – has been considered promising. This study aimed to determine which mitophagy-related signaling pathways (parkin, Bnip3, or FUNDC1) mediate the protective effects of postconditioning (PostC) and melatonin, both of which enhance the intrinsic defense capacity of cerebral tissue. In addition, microRNA-137 and microRNA-145, as well as serum asprosin, a novel glucogenic adipokine, levels were analyzed in cerebral IR injury. Method: Rats were divided into four groups: control (sham), IR, IR+PostC and IR+Mel(n:10). After 90 minutes of occlusion, PostC was performed at the onset of reperfusion in three cycles of 30-sec reperfusion, followed by 10-sec ischemia. Results: All parameters involved in mitophagy pathways increased with IR in cerebral cortex, and serum asprosin level decreased. Parkin and PINK1 levels did not change due to the treatments, while the FUNDC1 and Bnip3 levels decreased and serum asprosin levels increased significantly compared to IR. MicroRNA-137 and microRNA-145 decreased, although treatment partially restored the levels of these microRNAs. Conclusion: Increased expressions of parkin/PINK1, FUNDC1 and Bnip3 may suggest that all mitophagy pathways are activated by cerebral IR. Melatonin PostC may protect the cerebral tissue by inhibiting BNİP3- and FUNDC1-mediated mitophagy. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Brain Injury is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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RecordInfo BibRecord:
  BibEntity:
    Identifiers:
      – Type: doi
        Value: 10.1080/02699052.2026.2638954
    Languages:
      – Code: eng
        Text: English
    PhysicalDescription:
      Pagination:
        PageCount: 11
        StartPage: 603
    Subjects:
      – SubjectFull: Adipokines
        Type: general
      – SubjectFull: Age of onset
        Type: general
      – SubjectFull: Autophagy
        Type: general
      – SubjectFull: Reperfusion injury
        Type: general
      – SubjectFull: Ischemia
        Type: general
      – SubjectFull: Research funding
        Type: general
      – SubjectFull: Data analysis
        Type: general
      – SubjectFull: MicroRNA
        Type: general
      – SubjectFull: Polymerase chain reaction
        Type: general
      – SubjectFull: Enzyme-linked immunosorbent assay
        Type: general
      – SubjectFull: Parameters (Statistics)
        Type: general
      – SubjectFull: Melatonin
        Type: general
      – SubjectFull: Cellular signal transduction
        Type: general
      – SubjectFull: Descriptive statistics
        Type: general
      – SubjectFull: Mitochondrial proteins
        Type: general
      – SubjectFull: Rats
        Type: general
      – SubjectFull: Experimental design
        Type: general
      – SubjectFull: Cerebral cortex
        Type: general
      – SubjectFull: Mathematical statistics
        Type: general
      – SubjectFull: Animal experimentation
        Type: general
      – SubjectFull: Cardiovascular surgery
        Type: general
      – SubjectFull: One-way analysis of variance
        Type: general
      – SubjectFull: Statistics
        Type: general
      – SubjectFull: Neuropsychological tests
        Type: general
      – SubjectFull: Western immunoblotting
        Type: general
      – SubjectFull: Cerebral ischemia
        Type: general
      – SubjectFull: Cell survival
        Type: general
      – SubjectFull: Membrane proteins
        Type: general
      – SubjectFull: Biomarkers
        Type: general
      – SubjectFull: Turkey
        Type: general
    Titles:
      – TitleFull: The protective effects of melatonin postconditioning in cerebral ischemia may be mediated through the modulation of FUNDC1 and Bnip3 levels.
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            – D: 01
              M: 05
              Text: 2026
              Type: published
              Y: 2026
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