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Endoplasmic reticulum stress-related neuroinflammation and neural stem cells decrease in mice exposure to paraquat.

Zhengli Yang1, Yiming Shao1, Yifan Zhao1

  • 1School of Public Health/MOE Key Laboratory of Public Health Safety/NHC Key Lab of Health Technology Assessment, Fudan University, 130 Dong'an Road, Shanghai, 200032, China.

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This summary is machine-generated.

Paraquat herbicide exposure reduces neural stem cells (NSCs) by inducing endoplasmic reticulum (ER) stress in microglia, leading to neuroinflammation and impaired NSC proliferation. Tauroursodeoxycholic Acid (TUDCA) intervention showed potential therapeutic effects.

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Area of Science:

  • Neuroscience
  • Toxicology
  • Stem Cell Biology

Background:

  • Paraquat (PQ) is a widely used herbicide linked to neurodegenerative diseases.
  • The precise mechanisms underlying PQ neurotoxicity, particularly its effects on neural stem cells (NSCs), are not fully understood.
  • Investigating the role of endoplasmic reticulum (ER) stress and neuroinflammation in PQ-induced NSC impairment is crucial.

Purpose of the Study:

  • To investigate the direct impact of paraquat (PQ) on neural stem cells (NSCs) in vivo.
  • To elucidate the underlying mechanisms of PQ-induced neurotoxicity, focusing on ER stress and neuroinflammation.
  • To evaluate the therapeutic potential of Tauroursodeoxycholic Acid (TUDCA) in mitigating PQ's effects.

Main Methods:

  • Adult C57BL/6 mice were administered PQ (2 mg/kg or 20 mg/kg) or vehicle weekly for two weeks.
  • Neural stem cell (NSC) numbers, proliferation, and apoptosis were assessed in the subgranular zone (SGZ) and subventricular zone (SVZ).
  • ER stress in microglia and neuroinflammation were analyzed, with additional experiments using an ER stress inhibitor and TUDCA intervention.

Main Results:

  • A dose of 20 mg/kg PQ significantly decreased NSC numbers in the SGZ and SVZ by suppressing proliferation, without affecting apoptosis.
  • PQ exposure induced ER stress in microglia and caused significant neuroinflammation in the SGZ and SVZ.
  • Inhibition of ER stress ameliorated both neuroinflammation and the reduction in NSC numbers.

Conclusions:

  • Increased ER stress in microglia is identified as a potential key pathway mediating paraquat-induced neuroinflammation and neural stem cell (NSC) impairment.
  • This study reveals a novel mechanism for paraquat neurotoxicity.
  • The findings suggest that targeting ER stress may offer a therapeutic strategy against paraquat-induced neurotoxicity.