Physcion Mitigates LPS-Induced Neuroinflammation, Oxidative Stress, and Memory Impairments via TLR-4/NF-кB Signaling in Adult Mice

Sareer Ahmad, Kyonghwan Choe, Haroon Badshah, Riaz Ahmad, Waqar Ali, Inayat Ur Rehman, Tae Ju Park, Jun Sung Park, Myeong Ok Kim*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Alzheimer’s disease (AD) is the most predominant cause of dementia, considered a progressive decline in cognitive function that ultimately leads to death. AD has posed a substantial challenge in the records of medical science over the past century, representing a predominant etiology of dementia with a high prevalence rate. Neuroinflammation is a common characteristic of various central nervous system (CNS) pathologies like AD, primarily mediated by specialized brain immune and inflammatory cells, such as astrocytes and microglia. The present study aims to elucidate the potential mechanism of physcion that mitigates LPS-induced gliosis and assesses oxidative stress in mice. Physcion reduced the reactivity of Iba-1- and GFAP-positive cells and decreased the level of inflammatory cytokines like TNF-α and IL-1β. Physcion also reversed the effect of LPS-induced oxidative stress by upregulating the expression of Nrf2 and HO-1. Moreover, physcion treatment reversed LPS-induced synaptic disorder by increasing the level of presynaptic protein SNAP-23 and postsynaptic protein PSD-95. Our findings may provide a contemporary theoretical framework for clinical investigations aimed at examining the pathogenic mechanisms and therapeutic approaches for neuroinflammation and AD.

Original languageEnglish
Article number1199
JournalPharmaceuticals
Volume17
Issue number9
DOIs
Publication statusPublished - 11 Sept 2024

Keywords

  • Alzheimer’s disease (AD)
  • lipopolysaccharide (LPS)
  • neuroinflammation
  • oxidative stress
  • synapsis

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