Mitogen-activated protein kinase signaling is involved in nonylphenol-induced proinflammatory cytokines secretion by

Weijia Gu1, Yi Wang1, Zhenmin Qiu1

  • 1Department of Occupational and Environmental Health, School of Public Heath, China Medical University, Shenyang, People's Republic of China.

Insights

Nonylphenol (NP) exposure activates microglia (MG) inflammatory responses, increasing pro-inflammatory cytokines IL-6 and IL-1β. This occurs via the Akt/mitogen-activated protein kinase/activator protein 1 signaling pathway in the central nervous system.

Area of Science:

  • Neuroscience
  • Immunology
  • Toxicology

Background:

  • Microglia (MG) are central nervous system immune cells, crucial for innate immunity.
  • Microglia activation produces proinflammatory cytokines, contributing to inflammation and neurotoxicity.
  • Nonylphenol (NP), an endocrine disruptor, is known to impair neurodevelopment and memory.

Purpose of the Study:

  • To investigate the impact of nonylphenol (NP) on the inflammatory responses of BV2 microglia.
  • To elucidate the underlying molecular mechanisms by which NP influences microglia activation.

Main Methods:

  • BV2 microglia cells were treated with nonylphenol (NP).
  • Cytokine secretion (IL-6, IL-1β) was measured.
  • Protein phosphorylation (Akt, JNK, p38 MAPK, ERK) was analyzed.
  • Activator protein 1 (AP-1) activation was assessed.

Main Results:

  • Nonylphenol (NP) significantly increased the secretion of interleukin-6 (IL-6) and interleukin-1β (IL-1β) in BV2 microglia.
  • NP treatment led to increased phosphorylation of Akt, JNK, and p38 mitogen-activated protein kinase (MAPK).
  • NP exposure resulted in decreased phosphorylation of ERK and activation of the transcription factor activator protein 1 (AP-1).

Conclusions:

  • Nonylphenol (NP) provokes inflammatory responses in microglia.
  • NP activates the Akt/MAPK/AP-1 signaling pathway in microglia.
  • This activation leads to increased secretion of IL-6 and IL-1β, suggesting a role in neuroinflammation.

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