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Objective To study the effect ofβ?sodium aescinate on the expressions of aquaporin?4 and aquaporin?9 in rats with spinal cord inju?ry. Methods A total of 150 rats were randomly divided into 3 groups:sham group(n=50),spinal cord injury(SCI)group(n=50)andβ?sodi?um aescinate group(n=50). The experimental animal models was established by modified Allen’s model. The Basso,Beattie and Bresnahan (BBB)locomotor rating scale and inclined plane test were used to evaluate rat behavioral consequences after injury.The immunohistochemical staining and western blotting assay were performed to observe the expressions of aquaporin?4 and aquaporin?9. Results Compared with sham group,BBB score and inclined plane test score of SCI group andβ?sodium aescinate group were significantly lower at each time point(P<0.05);however,the functional recovery was significantly better inβ?sodium aescinate group than in SCI group at each time point from 7 d after SCI(P<0.05). The aquaporin?4 and aquaporin?9 positive expressions of rats in sham group were lower significantly than rats in SCI group andβ?sodium aescinate group(P<0.05);however,the aquaporin 4 and aquaporin 9 positive expressions of rats inβ?sodium aescinate group was lower signifi?cantly than rats in SCI group at each time point(P<0.05). Conclusion β?sodium aescinate can protect the neurologic function in rats with spi?nal cord injury by decreasing aquaporin?4 and aquaporin?9 protein expression.
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Objective To explore β-sodium aescinate on vascular endothelial function ( FMD ) , homocysteine ( Hcy ) and hypersensitive C-reactive protein ( hs-CRP) and clinical efficacy in patients with acute cerebral infarction.Methods 198 acute cerebral infarction patients from March 2013 to April 2015 were randomly divided into observation group (n=100) and control group (n=98).Control group were treated according to the condition of the disease, observation group were treated by β-sodium aescinate base on control group, 20mg was added to 250mL saline for intravenous drip,one times per day.Continuous used 14d for one treatment courses.Compared the change of vascular endothelial function, Hcy and hs-CRP and clinical efficacy.Results The total effective rate of observation group was 90.00%, which was significantly higher than that of 71.42% in control group (χ2 =11.01,P<0.05).Post-treatment the value of FMD significantly increased, Hcy and hs CRP were significantly decreased both in observation group and control group respectively, which the difference had a statistically significant as compared with Pre-treatment (P<0.05);but, the value of FMD was significantly higher, Hcy and hs CRP was significantly lower in observation group than that of control group (P<0.05).Conclusion It has a significant β-sodium aescinate clinical effect in treatment of acute cerebral infarction, and FMD are significantly higher, Hcy and hs-CRP are significantly decrease.
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Objective To investigate the expression of the hypoxia-inducible factor (HIF)-1α in rat brain neurons and the intervention of β-sodium aescinate after restoration of spontaneous circulation (ROSC).Methods Sixty SD adult rats were randomly (random number) divided into 3 groups (n =20),namely experiment group,control group and sham operation group.(1) The rats of experiment group were injected intraperitoneally with β-sodium aescinate (5 mg/kg) immediately after ROSC.(2) The rats of control group received normal saline injected intraperitoneally instead of β-sodium aescinate solution.(3)The rats of sham operation group did not have cardiac arrest and β-sodium aescinate intervention.Cardiac arrest rat model was established by using asphyxiation and intra-venous potassium chloride solution.Blood samples were taken 1 h,6 h,12 h and 24 h after ROSC,and subsequently rats were sacrificed and their brain tissues were harvested.The expressions of HIF-1 α mRNA,vascular endothelial growth factor (VEGF)mRNA and erythropoitin (EPO) mRNA and their protein levels in rat brain neurons were detected by using RT-PCR and immunohistochemistry,and the levels of serum neuron-specific enolase (NSE) and S100β proteins were determined by using enzyme-linked immunosorbent assay.The t test or one-way ANOVA was used to assess overall differences among groups for each of the variables,followed by Bonferroni test for multiple comparisons.Pearson method was used for correlation analysis.Results Compared with the sham operation group at intervals of 1 h,6 h,12 h and 24 h after ROSC,levels of serum S100β and NSE proteins were significantly increased in rats of the control group (P ＜ 0.05).Meanwhile,the expressions of HIF-1 α mRNA,VEGF mRNA and EPO mRNA and their protein levels in rat brain neurons were significantly increased in the control rats (P ＜0.05).Compared with the control group at intervals of 1 h,6 h,12 h and 24 h after ROSC,levels of serum NSE and S100β proteins were significantly decreased in rats of the experiment group (P ＜ 0.05).Whereas,the expressions of HIF-1 α mRNA,VEGF mRNA and EPO mRNA and their protein levels in rat brain neurons were significantly increased in rats of the experiment group (P ＜0.05).HIF-1 α mRNA was positively correlated with EPO mRNA and VEGF mRNAs (r =O.866,P ＜0.05 ; r =0.952,P ＜ O.01).Conclusions The expression of hypoxia-inducible factor-1 α is increased in rat brain cells after ROSC,and β-sodium aescinate up-regulates the expression of hypoxia-inducible factor1 α mRNA and protein levels.The up-regulated expression of hypoxia-inducible factor-1α improves the resistance of brain cells to ischemia and hypoxia contributing neuronal protection,which might be due to upregulated EPO and VEGF expressions induced by hypoxia-inducible factor-1α.
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BACKGROUND: This study was undertaken to investigate the expression of hypoxia-inducible factor-1α (HIF-1α) in rat cerebral cortex and the effects of β-sodium aescinate (SA) administration after return of spontaneous circulation (ROSC).METHODS: Sixty rats were divided into three groups: SA group, injected intraperitoneally with SA instantly after ROSC; control group, injected intraperitoneally with normal saline; and sham-operated group, without cardiac arrest or SA. The cardiac arrest model was established using asphyxiation and intravenous potassium chloride. Blood was sampled 1, 6, 12, and 24 hours after ROSC. Protein and mRNA levels of HIF-1α, VEGF and EPO were detected in the cerebral cortex by immunohistochemistry and real-time RT-PCR; serum levels of NSE and S100β were determined by enzyme-linked immunosorbent assays.RESULTS: Serum S100β and NSE were signifi cantly increased in the control group versus the sham-operated group 1, 6, 12 and 24 hours after ROSC (P<0.05). Protein and mRNA levels of HIF-1α, VEGF and EPO were signifi cantly increased in the control rats (P<0.05). Serum NSE and S100β were significantly decreased in the SA group versus the control group 1, 6, 12 and 24 hours after ROSC (P<0.05). Protein and mRNA levels of HIF-1α, VEGF and EPO were signifi cantly increased in the SA group (P<0.05).CONCLUSIONS: The expression of HIF-1α is increased in rat cerebral cortex after ROSC, and SA up-regulates the expression of HIF-1α. The up-regulation of HIF-1α improves the resistance of the cortex to ischemia and hypoxia and contributes to neuroprotection, possibly because of up-regulation of EPO and VEGF expression.