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Ghrelin improves cognitive function in diabetic rats by inhibiting the NF-κB pathway, reducing Aβ deposition, and mitigating oxidative stress. This brain-gut peptide targets the GHSR-1a receptor to achieve these neuroprotective effects.

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Area of Science:

  • Neuroscience
  • Endocrinology
  • Molecular Biology

Background:

  • Diabetes mellitus (DM) is associated with cognitive decline and increased amyloid-beta (Aβ) deposition in the hippocampus.
  • The brain-gut peptide Ghrelin plays a role in regulating cognitive function.
  • Understanding Ghrelin's molecular mechanisms in diabetic neurodegeneration is crucial.

Purpose of the Study:

  • To elucidate the molecular mechanisms by which Ghrelin improves cognitive function in diabetic rats.
  • To investigate Ghrelin's effect on Aβ deposition and oxidative stress in hippocampal neurons.
  • To explore Ghrelin's interaction with the GHSR-1a receptor and the NF-κB signaling pathway.

Main Methods:

  • Established a streptozotocin (STZ)-induced diabetic rat model.
  • Administered Ghrelin and GHSR-1a receptor antagonist (Dlys3-GHRP-6).
  • Assessed learning and memory using the Morris Water Maze (MWM) test.
  • Analyzed hippocampal neuron ultrastructure, oxidative stress markers (MDA, ROS), Aβ levels, and key protein expressions (GHSR-1a, NF-κB, BACE1) via ELISA and Western blot.
  • Utilized primary cultured hippocampal neurons to simulate high glucose conditions and test interventions.

Main Results:

  • Diabetic rats exhibited impaired MWM performance, elevated MDA, ROS, and Aβ, alongside decreased GHSR-1a and PP1 expression.
  • Ghrelin treatment significantly improved MWM performance, reduced oxidative stress and Aβ deposition, and increased PP1 expression.
  • Ghrelin's beneficial effects were reversed by GHSR-1a receptor antagonists.
  • Ghrelin inhibited the IKK/NF-κB/BACE1 pathway, decreasing BACE1 and APP expression in high-glucose-treated neurons, an effect blocked by GHSR-1a and NF-κB inhibitors.

Conclusions:

  • Ghrelin enhances cognitive function in diabetic rats by binding to its receptor GHSR-1a.
  • Ghrelin activation inhibits the NF-κB pathway, leading to reduced BACE1 expression and Aβ deposition.
  • Ghrelin attenuates oxidative stress and improves learning and memory in diabetic conditions.