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Study · In vitro (cells) · 2025

7 results

[Regulatory Role of the AKT1/AMPK Pathway in Oxidative Stress of Lens Epithelial Cells in Cataract Patients].

Huang Y, Lyu B, Tang K, Hu K

Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition1 May 2025Cited by 1 (Europe PMC)

PMID40964109 (opens in a new tab)PMCIDPMC12439649 (opens in a new tab)DOI10.12182/20250560203 (opens in a new tab)PepBankPUB-40964109
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Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: CC BY-NC. Results still quote short attributed sentences.

Results from this study7

7 results from studies that gave the peptide. No result from this study comes from people.

  1. 01LabIn vitro (cells)Mechanism

    In stressed HLE-B3 cells with AKT1 knockdown, AICAR reversed the improvement in ROS levels relative to before treatment.

    In plain wordsIn cells with AKT1 knockdown, AICAR reversed the improvement in reactive oxygen levels compared with before treatment.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseROS levels
    Study

    humann: not reported in source

    HLE-B3 cells with oxidative stress and AKT1 knockdown
    Comparator
    Before AICAR treatment in AKT1-knockdown cells
    Outcome group
    Oxidative stress · Eye
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, compared with the findings before AICAR treatment, these effects were antagonized after AICAR treatment in the si-AKT1 group (all P < 0.05).
    5 context sentences
    Summary · context
    Compared to those in the si-NC group, these indicators were improved in the si-AKT1 group (all P < 0.05).
    Summary · context
    Compared with the control + si-NC group, the si-NC group exhibited elevated ROS and MDA levels, increased apoptosis rate, reduced SOD and GSH levels, downregulated Bcl-2, and upregulated Bax (all P < 0.05).
    Summary · context
    2) An oxidative stress model of lens epithelial cells was established by treating HLE-B3 cells with 200 μmol/L H2O2 for 24 h.
    Summary · context
    A si-AKT1 parallel group demonstrating significant changes in p-AMPK/AMPK values was selected and treated with Acadesine (AICAR), an AMPK agonist, to verify the role of the AMPK pathway.
    Summary · context
    Western blot was performed to determine Bcl-2 and Bax protein levels in the si-NC group, the control + si-NC group, and the si-AKT1 group before and after the administration of AICAR.
  2. 02LabIn vitro (cells)Mechanism

    In stressed HLE-B3 cells with AKT1 knockdown, AICAR reversed the improvement in MDA levels relative to before treatment.

    In plain wordsIn cells with AKT1 knockdown, AICAR reversed the improvement in MDA levels compared with before treatment.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseMDA levels
    Study

    humann: not reported in source

    HLE-B3 cells with oxidative stress and AKT1 knockdown
    Comparator
    Before AICAR treatment in AKT1-knockdown cells
    Outcome group
    Oxidative stress · Eye
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, compared with the findings before AICAR treatment, these effects were antagonized after AICAR treatment in the si-AKT1 group (all P < 0.05).
    5 context sentences
    Summary · context
    Compared to those in the si-NC group, these indicators were improved in the si-AKT1 group (all P < 0.05).
    Summary · context
    Compared with the control + si-NC group, the si-NC group exhibited elevated ROS and MDA levels, increased apoptosis rate, reduced SOD and GSH levels, downregulated Bcl-2, and upregulated Bax (all P < 0.05).
    Summary · context
    2) An oxidative stress model of lens epithelial cells was established by treating HLE-B3 cells with 200 μmol/L H2O2 for 24 h.
    Summary · context
    A si-AKT1 parallel group demonstrating significant changes in p-AMPK/AMPK values was selected and treated with Acadesine (AICAR), an AMPK agonist, to verify the role of the AMPK pathway.
    Summary · context
    Western blot was performed to determine Bcl-2 and Bax protein levels in the si-NC group, the control + si-NC group, and the si-AKT1 group before and after the administration of AICAR.
  3. 03LabIn vitro (cells)Mechanism

    In stressed HLE-B3 cells with AKT1 knockdown, AICAR reversed the reduction in apoptosis relative to before treatment.

    In plain wordsIn cells with AKT1 knockdown, AICAR reversed the reduction in cell death compared with before treatment.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseApoptosis rate
    Study

    humann: not reported in source

    HLE-B3 cells with oxidative stress and AKT1 knockdown
    Comparator
    Before AICAR treatment in AKT1-knockdown cells
    Outcome group
    Cell viability and death · Eye
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, compared with the findings before AICAR treatment, these effects were antagonized after AICAR treatment in the si-AKT1 group (all P < 0.05).
    5 context sentences
    Summary · context
    Compared to those in the si-NC group, these indicators were improved in the si-AKT1 group (all P < 0.05).
    Summary · context
    Compared with the control + si-NC group, the si-NC group exhibited elevated ROS and MDA levels, increased apoptosis rate, reduced SOD and GSH levels, downregulated Bcl-2, and upregulated Bax (all P < 0.05).
    Summary · context
    2) An oxidative stress model of lens epithelial cells was established by treating HLE-B3 cells with 200 μmol/L H2O2 for 24 h.
    Summary · context
    A si-AKT1 parallel group demonstrating significant changes in p-AMPK/AMPK values was selected and treated with Acadesine (AICAR), an AMPK agonist, to verify the role of the AMPK pathway.
    Summary · context
    Western blot was performed to determine Bcl-2 and Bax protein levels in the si-NC group, the control + si-NC group, and the si-AKT1 group before and after the administration of AICAR.
  4. 04LabIn vitro (cells)Mechanism

    In stressed HLE-B3 cells with AKT1 knockdown, AICAR reversed the improvement in SOD levels relative to before treatment.

    In plain wordsIn cells with AKT1 knockdown, AICAR reversed the improvement in SOD levels compared with before treatment.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseSOD levels
    Study

    humann: not reported in source

    HLE-B3 cells with oxidative stress and AKT1 knockdown
    Comparator
    Before AICAR treatment in AKT1-knockdown cells
    Outcome group
    Oxidative stress · Eye
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, compared with the findings before AICAR treatment, these effects were antagonized after AICAR treatment in the si-AKT1 group (all P < 0.05).
    5 context sentences
    Summary · context
    Compared to those in the si-NC group, these indicators were improved in the si-AKT1 group (all P < 0.05).
    Summary · context
    Compared with the control + si-NC group, the si-NC group exhibited elevated ROS and MDA levels, increased apoptosis rate, reduced SOD and GSH levels, downregulated Bcl-2, and upregulated Bax (all P < 0.05).
    Summary · context
    2) An oxidative stress model of lens epithelial cells was established by treating HLE-B3 cells with 200 μmol/L H2O2 for 24 h.
    Summary · context
    A si-AKT1 parallel group demonstrating significant changes in p-AMPK/AMPK values was selected and treated with Acadesine (AICAR), an AMPK agonist, to verify the role of the AMPK pathway.
    Summary · context
    Western blot was performed to determine Bcl-2 and Bax protein levels in the si-NC group, the control + si-NC group, and the si-AKT1 group before and after the administration of AICAR.
  5. 05LabIn vitro (cells)Mechanism

    In stressed HLE-B3 cells with AKT1 knockdown, AICAR reversed the improvement in GSH levels relative to before treatment.

    In plain wordsIn cells with AKT1 knockdown, AICAR reversed the improvement in GSH levels compared with before treatment.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseGSH levels
    Study

    humann: not reported in source

    HLE-B3 cells with oxidative stress and AKT1 knockdown
    Comparator
    Before AICAR treatment in AKT1-knockdown cells
    Outcome group
    Oxidative stress · Eye
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, compared with the findings before AICAR treatment, these effects were antagonized after AICAR treatment in the si-AKT1 group (all P < 0.05).
    5 context sentences
    Summary · context
    Compared to those in the si-NC group, these indicators were improved in the si-AKT1 group (all P < 0.05).
    Summary · context
    Compared with the control + si-NC group, the si-NC group exhibited elevated ROS and MDA levels, increased apoptosis rate, reduced SOD and GSH levels, downregulated Bcl-2, and upregulated Bax (all P < 0.05).
    Summary · context
    2) An oxidative stress model of lens epithelial cells was established by treating HLE-B3 cells with 200 μmol/L H2O2 for 24 h.
    Summary · context
    A si-AKT1 parallel group demonstrating significant changes in p-AMPK/AMPK values was selected and treated with Acadesine (AICAR), an AMPK agonist, to verify the role of the AMPK pathway.
    Summary · context
    Western blot was performed to determine Bcl-2 and Bax protein levels in the si-NC group, the control + si-NC group, and the si-AKT1 group before and after the administration of AICAR.
  6. 06LabIn vitro (cells)Mechanism

    In stressed HLE-B3 cells with AKT1 knockdown, AICAR reversed the improvement in Bcl-2 expression relative to before treatment.

    In plain wordsIn cells with AKT1 knockdown, AICAR reversed the improvement in Bcl-2 expression compared with before treatment.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseBcl-2 expression
    Study

    humann: not reported in source

    HLE-B3 cells with oxidative stress and AKT1 knockdown
    Comparator
    Before AICAR treatment in AKT1-knockdown cells
    Outcome group
    Cell viability and death · Eye
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, compared with the findings before AICAR treatment, these effects were antagonized after AICAR treatment in the si-AKT1 group (all P < 0.05).
    5 context sentences
    Summary · context
    Compared to those in the si-NC group, these indicators were improved in the si-AKT1 group (all P < 0.05).
    Summary · context
    Compared with the control + si-NC group, the si-NC group exhibited elevated ROS and MDA levels, increased apoptosis rate, reduced SOD and GSH levels, downregulated Bcl-2, and upregulated Bax (all P < 0.05).
    Summary · context
    2) An oxidative stress model of lens epithelial cells was established by treating HLE-B3 cells with 200 μmol/L H2O2 for 24 h.
    Summary · context
    A si-AKT1 parallel group demonstrating significant changes in p-AMPK/AMPK values was selected and treated with Acadesine (AICAR), an AMPK agonist, to verify the role of the AMPK pathway.
    Summary · context
    Western blot was performed to determine Bcl-2 and Bax protein levels in the si-NC group, the control + si-NC group, and the si-AKT1 group before and after the administration of AICAR.
  7. 07LabIn vitro (cells)Mechanism

    In stressed HLE-B3 cells with AKT1 knockdown, AICAR reversed the improvement in Bax expression relative to before treatment.

    In plain wordsIn cells with AKT1 knockdown, AICAR reversed the improvement in Bax expression compared with before treatment.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseBax expression
    Study

    humann: not reported in source

    HLE-B3 cells with oxidative stress and AKT1 knockdown
    Comparator
    Before AICAR treatment in AKT1-knockdown cells
    Outcome group
    Cell viability and death · Eye
    Studied dose
    Dose not stated

    Source sentences

    Summary
    However, compared with the findings before AICAR treatment, these effects were antagonized after AICAR treatment in the si-AKT1 group (all P < 0.05).
    5 context sentences
    Summary · context
    Compared to those in the si-NC group, these indicators were improved in the si-AKT1 group (all P < 0.05).
    Summary · context
    Compared with the control + si-NC group, the si-NC group exhibited elevated ROS and MDA levels, increased apoptosis rate, reduced SOD and GSH levels, downregulated Bcl-2, and upregulated Bax (all P < 0.05).
    Summary · context
    2) An oxidative stress model of lens epithelial cells was established by treating HLE-B3 cells with 200 μmol/L H2O2 for 24 h.
    Summary · context
    A si-AKT1 parallel group demonstrating significant changes in p-AMPK/AMPK values was selected and treated with Acadesine (AICAR), an AMPK agonist, to verify the role of the AMPK pathway.
    Summary · context
    Western blot was performed to determine Bcl-2 and Bax protein levels in the si-NC group, the control + si-NC group, and the si-AKT1 group before and after the administration of AICAR.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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