Abstract

Objective To investigate the effects of ginkgolide B on neuronal cell apoptosis,superoxide dismutase activity,malondialdehyde,interleukin-1beta,tumor necrosis factor-alpha,and interleukin-6 levels in serum of rats with intracerebral hemorrhage in order to explore the role of ginkgolide B in suppressing the neuronal cell apoptosis.Methods A total of 175 male Wistar rats were randomly (random number)divided into sham operation group,intracerebral hemorrhage group,as well as low,medium and high dose treatment groups.The rat model of intracerebral hemorrhage was made with infusion of autologous whole blood to caudate nucleus in the right basal ganglia region.Ginkgolide B in dose of 5 mg/kg,10 mg/kg and 20 mg/kg was given to rats in the low,middle and high dose treatment groups by intraperitoneal injection once a day for 5 days after intracerebral hemorrhage.The rats with intracerebral hemorrhage in the sham operation groups received intraperitoneal administration of 1 mL saline.Animals were sacrificed by decapitation 2,6,12,24,48,72 h and 5 days after intracerebral hemorrhage.Brains were taken and blood samples were collected.Neuronal cell apoptosis was measured by using terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling(TUNEL),and superoxide dismutase activity in serum was determined by using xanthine oxidase method,and serum malondialdehyde level was detected by using thiobarbituric acid reactive substance assay,and interleukin-1beta,tumor necrosis factor-alpha,and interleukin-6 levels in serum were assayed with enzyme linked immunosorbent assay(ELISA).Statistical analysis was carried out by using one-way analysis of variance and least-significant difference test.Results As 2 h,6 h,12 h,24 h,48 h,72 h,and 5 days after intracerebral hemorrhage,the differences in the number of apoptotic neuronal cell,superoxide dismutase activity in serum,serum malondialdehyde,interleukin-1 beta,tumor necrosis factor-alpha and interleukin-6 levels between the low dose treatment group and intracerebral hemorrhage group were not significant statistically(P >0.05).As 12 h,24 h,72 h,and 5 days after intracerebral hemorrhage,the number of apoptotic neuronal cell,superoxide dismutase activity in serum,serum malondialdehyde,interleukin-1 beta,tumor necrosis factor-alpha and interleukin-6 levels in the medium dose and high dose treatment groups were significantly statistically lower than those in the intracerebral hemorrhage group(P < 0.05),but these differences in above biomarkers were not significant statistically among these three groups 2 and 6 hours after intracerebral hemorrhage(P > 0.05).Conclusions Ginkgolide B may lessen neuronal cell apoptosis by means of inhibition of free radical production and inflammatory reactions after intracerebral hemorrhage. Key words: Intracerebral hemorrhage; Ginkgolide B; Apoptosis; Free radical; Inflammation

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