TY - JOUR
T1 - Reduction of cerebral infarction in rats by biliverdin associated with amelioration of oxidative stress
AU - Deguchi, Kentaro
AU - Hayashi, Takeshi
AU - Nagotani, Shoko
AU - Sehara, Yoshihide
AU - Zhang, Han Zhe
AU - Tsuchiya, Atsushi
AU - Ohta, Yasuyuki
AU - Tomiyama, Koji
AU - Morimoto, Nobutoshi
AU - Miyazaki, Masahiro
AU - Huh, Nam ho
AU - Nakao, Atsunori
AU - Kamiya, Tatsushi
AU - Abe, Koji
N1 - Funding Information:
This work was partly supported by Grant-in-Aid for Scientific Research (B) 15390273 and (Hoga) 17659445 and National Project on Protein Structural and Functional Analyses from the Ministry of Education, Science, Culture and Sports of Japan and by grants (Itoyama Y, Imai T and Kuzuhara S) from the Ministry of Health and Welfare of Japan.
PY - 2008/1/10
Y1 - 2008/1/10
N2 - 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.
AB - 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.
KW - Biliverdin
KW - Brain ischemia
KW - Free radical scavenger
KW - Oxidative stress
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U2 - 10.1016/j.brainres.2007.07.104
DO - 10.1016/j.brainres.2007.07.104
M3 - Article
C2 - 18035335
AN - SCOPUS:37349048899
SN - 0006-8993
VL - 1188
SP - 1
EP - 8
JO - Molecular Brain Research
JF - Molecular Brain Research
IS - 1
ER -