Reduction of cerebral infarction in rats by biliverdin associated with amelioration of oxidative stress

Kentaro Deguchi, Takeshi Hayashi, Shoko Nagotani, Yoshihide Sehara, Han Zhe Zhang, Atsushi Tsuchiya, Yasuyuki Ohta, Koji Tomiyama, Nobutoshi Morimoto, Masahiro Miyazaki, Nam ho Huh, Atsunori Nakao, Tatsushi Kamiya, Koji Abe

Research output: Contribution to journalArticlepeer-review

55 Citations (Scopus)


Biliverdin (BV), one of the byproducts of heme catalysis through heme oxygenase (HO) system, is a scavenger of reactive oxygen species (ROS). We hypothesized that BV treatment could protect rat brain cells from oxidative injuries via its anti-oxidant efficacies. Cerebral infarction was induced by transient middle cerebral artery occlusion (tMCAO) for 90 min, followed by reperfusion. BV or vehicle was administered intraperitoneally immediately after reperfusion. The size of the cerebral infarction 2 days after tMCAO was evaluated by 2,3,5-triphenyltetrazolium chloride (TTC) stain. Superoxide generation 4 h after tMCAO was determined by detection of oxidized hydroethidine. In addition, the oxidative impairment of neurons were immunohistochemically assessed by stain for lipid peroxidation with 4-hydroxy-2-nonenal (4-HNE) and damaged DNA with 8-hydroxy-2′-deoxyguanosine (8-OHdG). BV treatment significantly reduced infarct volume of the cerebral cortices associated with less superoxide production and decreased oxidative injuries of brain cells. The present study demonstrated that treatment with BV ameliorated the oxidative injuries on neurons and decreased brain infarct size in rat tMCAO model.

Original languageEnglish
Pages (from-to)1-8
Number of pages8
JournalBrain Research
Issue number1
Publication statusPublished - Jan 10 2008
Externally publishedYes


  • Biliverdin
  • Brain ischemia
  • Free radical scavenger
  • Oxidative stress

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology


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