Biomolecular and Functional Changes in a Culture of Microglial Cells Caused by Long-Term Exposure to AlCl3

A V Sentyabreva1,2, M A Diatroptova3, E A Miroshnichenko3,4

  • 1Avtsyn Research Institute of Human Morphology, Petrovsky National Research Centre of Surgery, Moscow, Russia. alexandraasentyabreva@gmail.com.

Insights

Aluminum chloride (AlCl3) exposure in microglia cells can model inflammaging. Lower AlCl3 concentrations suggest healthy aging, while higher concentrations induce persistent microglial activation, crucial for age-related disease research.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Inflammaging, a chronic proinflammatory state, drives age-related diseases.
  • Microglial cells, key immune cells in the brain, become activated and dysfunctional due to increased reactive oxygen species (ROS) and inflammation.
  • Aluminum chloride (AlCl3) is a prooxidant that may influence microglial aging.

Purpose of the Study:

  • To investigate the biomolecular and functional effects of long-term aluminum chloride exposure on microglial cells.
  • To model inflammaging and associated cellular changes in vitro.
  • To determine the dose-dependent effects of AlCl3 on microglial activation and phenotype.

Main Methods:

  • BV2 microglial cell line cultured with 0.5 mM and 1 mM AlCl3 for 70 or 140 hours.
  • Assessment of reactive oxygen species (ROS) production via flow cytometry.
  • Evaluation of apoptosis and M1/M2 phenotype polarization using qPCR-RT and ELISA.

Main Results:

  • Low-dose AlCl3 (0.5 mM) exposure resulted in characteristics of "healthy aging" in microglia.
  • High-dose AlCl3 (1 mM) induced persistent activation and dysfunction of microglial cells.
  • AlCl3 exposure modulated ROS production, apoptosis, and M1/M2 polarization.

Conclusions:

  • Aluminum chloride can be used to create an in vitro model of inflammaging.
  • Microglial responses to AlCl3 are concentration-dependent, mimicking aspects of aging.
  • This model aids in studying age-related diseases linked to microglial dysfunction.