Effect of edaravone on inflammatory factors 6-keto-prostaglandin F1α, thromboxane B2, endothelial function, copeptin and N-terminal brain natriuretic peptide in patients with acute cerebral infarction / 中国生化药物杂志

ABSTRACT

Objective To investigate effect of edaravone on serum inflammatory factors, 6-keto-prostaglandin F1α(6-keto-PGF1α), thromboxane B2, endothelial function and serum copeptin and N-terminal brain natriuretic peptide (NT-proBNP) in patients with acute cerebral infarction.Methods From March 2013 to September 2014, 213 cases of acute cerebral infarction were selected in the hospital and randomly divided into control group (n=101) and observation group (n =112).Control group were given conventional symptomatic treatment, and observation group were given edaravone injection on the basis of control group.The serum inflammatory cytokines, 6-keto-PGF1α, thromboxane B2, endothelial function, serum copeptin, NT-proBNP and nerve function score and activities of daily living ( ADL) score were compared between two groups.Results Serum CRP, IL-8, IL-10 in observation group after treatment were significantly lower than control group (P<0.05).Plasma thromboxane B2 in observation group after treatment was significantly lower than control group (P<0.05).The levels of 6-keto-PGF1αwas significantly higher than control group (P<0.05).Serum copeptin and NT-proBNP levels in observation group after treatment were significantly lower than control group (P<0.05).Plasma ET-1 in observation group after treatment was significantly lower than control group ( P<0.05 ) , and plasma NO was significantly higher than the control ( P<0.05 ).Neurological function in observation group after treatment was significantly lower than control group (P<0.05), and ADL score was significantly higher (P<0.05). Conclusion The preliminary study shows that edaravone in treatment of acute cerebral infarction may be associated with decreasing serum inflammatory cytokines, increasing 6-keto-PGF1αand reducing thromboxane B2, improving endothelial function and reducing serum copeptin and N-terminal natriuretic peptide.