2 min read

ID: 925708

Short Link: https://gregory-ms.com/articles/925708/

Discovery Date: 21 September 2022, 11:50:08 UTC

Published Date: 2022-09-20 23:00:00

Source: BioMedCentral

Link: https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-022-02596-7

Manual Selection: true

Machine Learning Gaussian Naive Bayes Model: false


jats:titleAbstract</jats:title>jats:sec jats:titleBackground</jats:title> jats:pRadiation-induced brain injury (RIBI) is the most serious complication of radiotherapy in patients with head and neck tumors, which seriously affects the quality of life. Currently, there is no effective treatment for patients with RIBI, and identifying new treatment that targets the pathological mechanisms of RIBI is urgently needed.</jats:p> </jats:sec>jats:sec jats:titleMethods</jats:title> jats:pImmunofluorescence staining, western blotting, quantitative real-time polymerase chain reaction (Q-PCR), co-culture of primary neurons and microglia, terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay, enzyme-linked immunosorbent assay (ELISA), and CRISPR–Cas9-mediated gene editing techniques were employed to investigate the protective effects and underlying mechanisms of pregabalin that ameliorate microglial activation and neuronal injury in the RIBI mouse model.</jats:p> </jats:sec>jats:sec jats:titleResults</jats:title> jats:pOur findings showed that pregabalin effectively repressed microglial activation, thereby reducing neuronal damage in the RIBI mouse model. Pregabalin mitigated inflammatory responses by directly inhibiting cytoplasmic translocation of high-mobility group box 1 (HMGB1), a pivotal protein released by irradiated neurons which induced subsequent activation of microglia and inflammatory cytokine expression. Knocking out neuronal HMGB1 or microglial TLR2/TLR4/RAGE by CRISPR/Cas9 technique significantly inhibited radiation-induced NF-κB activation and pro-inflammatory transition of microglia.</jats:p> </jats:sec>jats:sec jats:titleConclusions</jats:title> jats:pOur findings indicate the protective mechanism of pregabalin in mitigating microglial activation and neuronal injury in RIBI. It also provides a therapeutic strategy by targeting HMGB1-TLR2/TLR4/RAGE signaling pathway in the microglia for the treatment of RIBI.</jats:p> </jats:sec>

Noun Phrases in Title

  • Pregabalin
  • microglial activation
  • neuronal injury
  • HMGB1
  • pathway
  • radiation-induced brain injury
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