Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Benzene to 1,4-Cyclohexadiene: Birch Reduction Mechanism01:18

Benzene to 1,4-Cyclohexadiene: Birch Reduction Mechanism

2.2K
Birch reduction uses solvated electrons as reducing agents. The reaction converts benzene to 1,4-cyclohexadiene. The reaction proceeds by the transfer of a single electron to the ring to form a benzene radical anion. This anion is highly basic—it abstracts a proton from the alcohol to form a cyclohexadienyl radical. Another single electron transfer gives the cyclohexadienyl anion. A proton transfer from the alcohol forms 1,4-cyclohexadiene. Since this reduction occurs via radical anion...
2.2K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Corrigendum to "Neuroprotection by post-stroke administration of the slow-releasing hydrogen sulfide (H2S) donor AP39: Long-term functional, MRI, and molecular evidence in a rodent stroke model" [European J. Pharmacol. 1008 (2025) 178331].

European journal of pharmacology·2026
Same author

Nitazoxanide reduces atherosclerosis by decreasing polarization of macrophages to proinflammatory M1 phenotype via inhibition of NF-κB pathway.

Biochemical pharmacology·2026
Same author

Cortical thinning and volumetric alterations in patients with unruptured intracranial aneurysms: insights from surface-based morphometry.

Neurosurgical review·2026
Same author

Metallomic Aspects of Stroke and Recovery: ICP-MS Study with Chemometric Analysis.

Molecules (Basel, Switzerland)·2025
Same author

Can xenobiotics contribute to the increase in the incidence of endocrine diseases by inducing autoimmune processes?

Folia medica Cracoviensia·2025
Same author

Effect of Aspirin Challenge on Innate Lymphoid Cells in Asthma Patients With Aspirin Hypersensitivity.

European journal of immunology·2025

Related Experiment Video

Updated: Jul 13, 2025

Microglia as a Surrogate Biosensor to Determine Nanoparticle Neurotoxicity
08:37

Microglia as a Surrogate Biosensor to Determine Nanoparticle Neurotoxicity

Published on: October 25, 2016

7.0K

Mechanism of Microglial Cell Activation in the Benzophenone-3 Exposure Model.

Alicja Maciejska1, Bartosz Pomierny1, Weronika Krzyżanowska1

  • 1Department of Toxicological Biochemistry, Faculty of Pharmacy, Jagiellonian University Medical College, Medyczna 9, 30-688 Kraków, Poland.

Neuroscience
|October 12, 2023
PubMed
Summary

Benzophenone-3 (BP-3), a common UV filter, alters microglial cell activation in rat brains, potentially impacting neuroinflammation. Exposure affects immune responses differently in the frontal cortex and hippocampus, suggesting complex neurological effects.

Keywords:
benzophenone-3cytokinesmicroglia activationmicroglia polarizationprimary microglia cells

More Related Videos

Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue
10:20

Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue

Published on: August 15, 2012

39.7K
Magnetic Isolation of Microglial Cells from Neonate Mouse for Primary Cell Cultures
07:23

Magnetic Isolation of Microglial Cells from Neonate Mouse for Primary Cell Cultures

Published on: July 25, 2022

3.1K

Related Experiment Videos

Last Updated: Jul 13, 2025

Microglia as a Surrogate Biosensor to Determine Nanoparticle Neurotoxicity
08:37

Microglia as a Surrogate Biosensor to Determine Nanoparticle Neurotoxicity

Published on: October 25, 2016

7.0K
Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue
10:20

Primary Microglia Isolation from Mixed Glial Cell Cultures of Neonatal Rat Brain Tissue

Published on: August 15, 2012

39.7K
Magnetic Isolation of Microglial Cells from Neonate Mouse for Primary Cell Cultures
07:23

Magnetic Isolation of Microglial Cells from Neonate Mouse for Primary Cell Cultures

Published on: July 25, 2022

3.1K

Area of Science:

  • Neuroscience
  • Toxicology
  • Immunology

Background:

  • Benzophenone-3 (BP-3) is a widely used cosmetic UV filter, known to penetrate the skin and blood-brain barrier.
  • BP-3 has been linked to increased glutamate, lipid peroxidation, microglial proliferation, and apoptosis in brain tissue.
  • Microglial cells are crucial immune cells in the central nervous system, responding to injury and inflammation.

Purpose of the Study:

  • To investigate the effects of prenatal and adult exposure to Benzophenone-3 (BP-3) on microglial cell activation and polarization.
  • To compare the impact of BP-3 on microglial cells in the frontal cortex and hippocampus of adult male rats.
  • To elucidate the mechanisms underlying BP-3-induced neuroinflammation, including cytokine production and receptor expression.

Main Methods:

  • Adult male rats were exposed to BP-3 prenatally and for two weeks in adulthood.
  • Analysis of microglial cell markers (M2 phenotype, CD86/CD206 ratio), transcription factors (NFκB), and enzymes (caspase-1) in brain tissues.
  • In vitro study using primary rat frontal cortical microglia cultures to assess cytokine release (IL-1α, IL-1β, TNFα, IL-6, IL-18, IP-10) with and without lipopolysaccharide (LPS) stimulation.

Main Results:

  • BP-3 exposure reduced M2 microglial markers in both frontal cortex and hippocampus.
  • Frontal cortex showed increased CD86/CD206 ratio, NFκB expression, and caspase-1 activity.
  • Hippocampus exhibited increased glucocorticoid receptor levels; in vitro studies revealed altered pro-inflammatory cytokine release, with BP-3 exacerbating LPS-induced responses.

Conclusions:

  • Prenatal and adult exposure to BP-3 significantly alters microglial cell activation and polarization in specific brain regions.
  • Differential effects on the frontal cortex and hippocampus suggest region-specific neuroinflammatory responses mediated by factors like glucocorticoid receptors.
  • BP-3 can exacerbate LPS-induced neuroinflammation by modulating cytokine production in microglia, indicating a potential risk for neurotoxicity.