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Urapidil as a neuroprotective agent: targeting hypoxia, inflammation, and oxidative stress in traumatic brain injury

Ahmet Bindal1, Pınar Karabacak1, Halil Asci2

  • 1Department of Anesthesiology and Reanimation, Faculty of Medicine, Suleyman Demirel University, Isparta, Türkiye.

European Journal of Trauma and Emergency Surgery : Official Publication of the European Trauma Society
|May 6, 2025
PubMed
Abstract

Insights

Urapidil (Ura) demonstrates significant neuroprotective effects against traumatic brain injury (TBI) in rats. It effectively reduces inflammation, oxidative stress, and cell death by modulating key molecular pathways, offering a promising therapeutic avenue for TBI.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Traumatic brain injury (TBI) is a leading cause of death and disability worldwide.
  • Current pharmaceutical treatments for TBI are insufficient, necessitating novel therapeutic strategies.
  • TBI involves complex mechanisms including inflammation, oxidative stress, and apoptosis.

Purpose of the Study:

  • To investigate the neuroprotective potential of Urapidil (Ura) in a rat model of TBI.
  • To evaluate the effects of Ura on molecular signaling pathways implicated in TBI pathogenesis, including HMGB1, BNIP3L, and HIF1α.

Main Methods:

  • Thirty-two rats were allocated into control, TBI, and TBI treated with two doses of Ura (0.5 mg/kg and 5 mg/kg).
  • Assessment of tissue integrity, inflammatory markers (TNF-α), apoptosis (caspase-3), and key signaling molecules (HIF1α, BNIP3L, HMGB1).
  • Evaluation of oxidative stress markers (TOS, OSI, TAS) following Ura treatment.

Main Results:

  • Ura treatment significantly reduced histopathological damage, expressions of BNIP3L, HMGB1, HIF1α, TNF-α, caspase-3, and tyrosine hydroxylase in TBI rats.
  • Ura administration also decreased oxidative stress markers (TOS, OSI) and increased antioxidant capacity (TAS).
  • These findings indicate Ura's ability to modulate neuroinflammation, mitochondrial dysfunction, and hypoxia pathways in TBI.

Conclusions:

  • Urapidil exhibits significant tissue-protective effects in a TBI model.
  • Ura effectively targets critical pathways involved in TBI, including inflammation, oxidative stress, and apoptosis.
  • Further research into Urapidil as a therapeutic agent for TBI is warranted.
Keywords:
ApoptosisInflammationNeuroprotectionRatTrauma

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