CCL5/RANTES signaling in inflammation dysregulation after mild traumatic brain injury.

ABSTRACT:

Background

Mild traumatic brain injury (mTBI) is the most prevalent form of brain injury. Secondary damage following mTBI contributes to neuronal degeneration by promoting neuroinflammation, amyloid accumulation, and oxidative stress (OS). Microglia exhibit dual roles after injury, contributing to both pro-inflammatory (M1) and anti-inflammation/neuroprotective (M2) responses. Targeting microglial polarization may therefore represent a therapeutic strategy for mitigating secondary damage after TBI.

Methods

A weight-drop mTBI model (30 g, 100 cm) was applied to both C57BL/6 (wild-type) and CCL5 knockout (CCL5-KO) mice. Microglial activation was assessed at 7-, 14-, 21-, and 28-days post-injury using RT-qPCR, immunohistochemistry, and western blotting. Oxidative stress in tiss

SUBMITTER: Ho MH 

PROVIDER: S-EPMC12784600 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature