ArticleJournal of biomedical science2026
CCL5/RANTES signaling in inflammation dysregulation after mild traumatic brain injury.
Article in Journal of biomedical science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundMild 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.
methodsA 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 tissue was detected by Hydroxyprobe™ labeling, ROS detection, NADPH oxidase activity assay, and antioxidant expression. Recombinant CCL5 (rCCL5) was administered intranasally to evaluate its effect on post-injury inflammation. Cortical tissue was subjected to liquid chromatography-tandem mass spectrometry (LC-MS/MS) for proteomic profiling. In vitro, BV2 microglial cells were treated with H
resultsrCCL5 significantly reduced oxidative stress in both neurons and microglia and enhanced expression of antioxidant enzymes such as GPX1, SOD1, and SOD2 in injured cortices. Proteomic analysis revealed upregulation of immune regulatory and phagocytosis-related pathways following rCCL5 treatment. In vitro, rCCL5 conferred cytoprotection against H
conclusionsThese findings demonstrate that CCL5 modulates microglial polarization and attenuates oxidative stress in the injured brain through a CCR5-dependent mechanism. Targeting the CCL5-CCR5 signaling axis may offer a promising therapeutic strategy for improving outcomes after mTBI.
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