NF-κB signaling modulates radiation‑induced microglial activation.

Area of Science:

• Neuroscience
• Immunology
• Radiation Biology

Background:

• Microglial activation is implicated in radiation-induced brain injury.
• The precise molecular mechanisms driving this activation remain incompletely understood.

Purpose of the Study:

• To investigate the molecular mechanisms underlying radiation-induced microglial activation.
• To explore the role of the nuclear factor-kappa B (NF-κB) signaling pathway in this process.

Main Methods:

• Mouse microglial BV-2 cells were exposed to varying radiation doses.
• Inflammatory factor release was measured using ELISA and RT-PCR.
• Protein expression and cellular changes were assessed via immunocytochemistry and immunoblotting.

Main Results:

• Radiation doses exceeding 16 Gray induced microglial activation, characterized by morphological changes and upregulation of ionized calcium-binding adapter molecule-1 and CD68.
• Key inflammatory factors (IL-1β, TNF-α, IL-6, TLR-8, COX-2) increased post-irradiation.
• Radiation exposure led to DNA double-strand breaks (γ-H2AX upregulation) and subsequent activation of the NF-κB pathway, indicated by p65 nuclear translocation and altered NEMO/IκB-α levels.

Conclusions:

• The NF-κB signaling pathway plays a critical role in triggering microglial activation and inflammatory factor release following irradiation.
• These findings offer insights into the molecular basis of radiation-induced brain injury, potentially informing therapeutic strategies.