Doxycycline alleviates acute traumatic brain injury by suppressing neuroinflammation and apoptosis in a mouse model

Marjani S., Zirh S., Sever-Bahcekapili M., Cakir-Aktas C., Muftuoglu S. F., Mut M.

JOURNAL OF NEUROIMMUNOLOGY, cilt.359, 2021 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 359
  • Basım Tarihi: 2021
  • Doi Numarası: 10.1016/j.jneuroim.2021.577672
  • Dergi Adı: JOURNAL OF NEUROIMMUNOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, CAB Abstracts, Chemical Abstracts Core, EMBASE, MEDLINE, Psycinfo, Veterinary Science Database
  • Anahtar Kelimeler: Traumatic brain injury, Neuroinflammation, Microglia, Doxycycline, RECRUITMENT, FLUID, NEUROPROTECTION, EXPRESSION, BIOMARKERS, REDUCTION, MEDIATORS, HEALTH, DAMAGE
  • Hacettepe Üniversitesi Adresli: Evet

Özet

Traumatic brain injury (TBI) is one of the significant causes of death among young people worldwide. Doxycycline (DOX), an antibiotic with anti-inflammatory effects, has not been used as a therapeutic agent to modify the inflammatory response after the traumatic brain injury. In this study, intraperitoneal administration of DOX reduced significantly the acute inflammatory markers like IL-6 and CD3, microglial migration to the damaged area marked with Iba-1, and neuronal apoptosis assessed with TUNEL assay at 72 h after the trauma. The low dose, 10 mg/kg of DOX had a dominant anti-inflammatory effect; while the high dose, 100 mg/kg of DOX, was more effective in decreasing neuronal apoptosis. In early hours after the head trauma, use of a low dose (10 mg/ kg) of DOX for decreasing the acute form of inflammation followed by a high dose (100 mg/kg) for the antiapoptotic effects particularly in severe head traumas, would be a promising approach to alleviate the brain injury.