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Basic Science and Pathogenesis.

Chia-Wen Tsai1, Han-Ting Wu1, Chun-Huei Liao1

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Carnosic acid (CA) protects against Bisphenol A (BPA) neuroinflammation by reducing oxidative stress and regulating key proteins. This study shows CA’s neuroprotective potential in both cell and animal models.

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Area of Science:

  • Neuroscience
  • Toxicology
  • Pharmacology

Background:

  • Bisphenol A (BPA) is an endocrine-disrupting chemical linked to neuroinflammation.
  • Microglial cell activation by BPA can lead to neuronal damage.
  • Rosemary-derived carnosic acid (CA) possesses antioxidant and neuroprotective properties.

Purpose of the Study:

  • To investigate the protective effects of carnosic acid (CA) against BPA-induced neuroinflammation and oxidative stress.
  • To evaluate CA's impact on inflammasome proteins and antioxidant enzymes.
  • To confirm CA's neuroprotective capacity in both in vitro and in vivo models.

Main Methods:

  • Human HMC3 microglia cells and C57BL/6J male mice were used.
  • Cells were treated with BPA and CA to assess neuroinflammation and oxidative stress markers.
  • Mice were administered BPA and varying doses of CA to evaluate in vivo effects.

Main Results:

  • CA treatment reversed BPA-induced increases in inflammasome proteins (NLRP3, caspase-1, IL-1β) and reactive oxygen species (ROS).
  • CA restored BPA-induced reductions in antioxidant enzymes, Nrf2, and UGT1A1.
  • In vivo studies confirmed CA's ability to restore antioxidant enzymes and UGT1A1 in the striatum.

Conclusions:

  • Carnosic acid (CA) demonstrates significant neuroprotection against BPA-induced neuroinflammation and oxidative stress.
  • CA exerts its effects by modulating inflammasome pathways and enhancing antioxidant defenses.
  • These findings highlight CA as a potential therapeutic agent for BPA-related neurological damage.