Temporin-GHaR Peptide Alleviates LPS-Induced Cognitive Impairment and Microglial Activation by Modulating Endoplasmic...

Area of Science:

• Neuroscience
• Immunology

Background:

• Neuroinflammation, driven by microglia, is a key factor in cognitive impairment.
• Endoplasmic reticulum stress (ERS) and NF-κB signaling are implicated in neuroinflammatory processes.

Purpose of the Study:

• To investigate the potential of temporin-GHaR peptide (GHaR) in improving cognitive function.
• To elucidate the underlying mechanisms of GHaR's effects on neuroinflammation and cognitive impairment.

Main Methods:

• In vivo studies using LPS-induced mouse models of cognitive impairment.
• In vitro experiments with BV2 microglial cells and neuronal cells.
• Assessment of microglial activation, ERS, NF-κB pathway, and inflammatory cytokine secretion (TNF-α, IL-6).

Main Results:

• GHaR treatment significantly alleviated LPS-induced cognitive impairment in mice.
• GHaR inhibited microglial activation, M1 polarization, and reduced TNF-α and IL-6 secretion.
• GHaR suppressed ERS and NF-κB signaling activation in both in vivo and in vitro models.
• GHaR protected neuronal cells from apoptosis induced by LPS-activated microglia.

Conclusions:

• GHaR demonstrates neuroprotective effects against LPS-induced cognitive impairment.
• GHaR attenuates neuroinflammation by reversing microglial activation.
• The neuroprotective mechanisms of GHaR involve the inhibition of endoplasmic reticulum stress (ERS) signaling.