Inhibition of brain damage by edaravone, a free radical scavenger, can be monitored by plasma biomarkers that detect oxidative and astrocyte damage in patients with acute cerebral infarction

• Published in: Free radical biology & medicine Vol. 39; no. 8; pp. 1109 - 1116
• Main Authors: Uno, Masaaki, Kitazato, Keiko T., Suzue, Atsuhiko, Matsuzaki, Kazuhito, Harada, Masahumi, Itabe, Hiroyuki, Nagahiro, Shinji
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 15-10-2005
• Subjects: Acute cerebral infarction; Adult; Aged; Aged, 80 and over; Antipyrine - analogs & derivatives; Antipyrine - therapeutic use; Astrocytes - pathology; Biomarkers - blood; Cerebral Infarction - drug therapy; Female; Free radical scavenger; Free Radical Scavengers - therapeutic use; Free radicals; Humans; Lipoproteins, LDL - blood; Male; Middle Aged; Monitoring, Physiologic; Nerve Growth Factors - blood; Oxidative Stress; Plasma biomarker; S100 Calcium Binding Protein beta Subunit; S100 Proteins - blood; Superoxide Dismutase - blood; Treatment Outcome; NIHSS; PWI; Free radicals; SOD; IR; Free radical scavenger; Acute cerebral infarction; mAb; MCAOR; Plasma biomarker; DWI; FLAIR; OxLDL; 8-OHdG
• ISSN: 0891-5849; 1873-4596
• DOI: 10.1016/j.freeradbiomed.2005.06.001

We assess the availability of plasma biomarkers to monitor the brain damage and the therapeutic efficacy of edaravone. The study consisted of 51 patients with ischemic cerebral infarcts. They were divided into 2 groups: GI (
n = 24) had cortical lesions, and GII (
n = 27) had lesions in the basal ganglia or brain stem. Edaravone was administered to 27 randomly selected patients (GIa,
n = 13; GIIa,
n = 14) and its efficacy was studied by comparing their plasma OxLDL, S-100B, and MnSOD levels to those in patients without edaravone (GIb,
n = 11, GIIb,
n = 13). Three days after the start of edaravone, plasma OxLDL was significantly lower in GIa than GIb patients (0.177 ± 0.024 ng/μg apoB vs 0.219 ± 0.026,
P < 0.05). In GIIa patients, pre- and posttreatment plasma OxLDL was not significantly different (0.156 ± 0.013 vs 0.152 ± 0.020). In GIa patients, S-100B and MnSOD were significantly lower than in GIb patients (
P < 0.05). The neurological condition at the time of discharge had recovered in GIa but not GIb patients. Ours is the first evidence to confirm the efficacy of edaravone by plasma biomarkers. In patients with cortical infarcts, edaravone reduced oxidative damage, thereby limiting the degree of brain damage.