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

• Published in: Probiotics and antimicrobial proteins
• Main Authors: Zhang, Da-Qi, Dong, Xiaoqian, Su, Simin, Zhang, Linlin, Zhang, Jiayu, Yang, Wenjing, Hu, Wenting, Li, Lushuang, Song, Yanting, Xie, Xi, Li, Qifu, Wang, Rong, Zhang, Yingxia
• Format: Journal Article
• Language: English
• Published: United States 11.05.2024
• Subjects: Neuroinflammation; Temporin-GHaR peptide; Cognitive impairment; Microglia
• ISSN: 1867-1306; 1867-1314
• DOI: 10.1007/s12602-024-10277-5

Neuroinflammation is considered an important factor that leads to cognitive impairment. Microglia play a crucial role in neuroinflammation, which leads to cognitive impairment. This study aimed at determining whether temporin-GHaR peptide (GHaR) could improve cognitive function and at uncovering the underlying mechanisms. We found that GHaR treatment alleviated LPS-induced cognitive impairment and inhibited activation of microglia in LPS-induced mice. Furthermore, GHaR inhibited activation of endoplasmic reticulum stress (ERS) and the NF-κB signaling pathway in LPS-induced mice. In vitro, GHaR inhibited M1 polarization of BV2 cells and suppressed TNF-α and IL-6 secretion. Additionally, GHaR neuronal cell viability and apoptosis were induced by LPS-activated microglia-conditioned medium. Moreover, in LPS-induced BV2 cells, GHaR inhibited activation of ERS and the NF-κB signaling pathway. In summary, GHaR improved LPS-induced cognitive and attenuated inflammatory responses via microglial activation reversal. In conclusion, the neuroprotective effects of GHaR were mediated via the ERS signaling pathway.