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OBJECTIVE:To investigate the therapeutic efficacy of edaravone combined with citicoline sodium on acute cere-bral infarction and its effects on the levels of oxidative stress and inflammatory factors. METHODS:108 patients with acute cere-bral infarction were randomly divided into edaravone group(single group)and edaravone+citicoline sodium group(drug combina-tion group),with 54 cases in each group. Based on routine treatment,single group was given Edaravone injection 30 mg added in-to 100 ml 0.9% Sodium chloride injection intravenously,bid,used up within 30 min each time;drug combination group was addi-tionally given Citicoline sodium injection 0.5 g added into 250 ml 0.9% Sodium chloride injection intravenously,qd,on the basis of single group. Treatment course of 2 groups lasted for 2 weeks. NIHSS,HDS,Barthel index,oxidant stress indicator and inflam-matory factors were compared between 2 groups before and after treatment. RESULTS:After treatment,the effective rate of NI-HSS in drug combination group was 81.48%,which was significantly higher than single group(53.70%),with statistical signifi-cance (χ2=9.511,P=0.002). HDS score and Barthel index of 2 groups were significantly increased after treatment,especially in drug combination group,with statistical significance(P<0.05). Compared with before treatment,contents of MDA and ET-1 in 2 groups were decreased significantly,while SOD activity and NO content were increased significantly;the inflammatory cytokines IL-6,IL-8,IL-12 and IL-16,TNF-α were all decreased gradually,with statistical significance (P<0.05);the improvement of each indicator in drug combination group was more significant than single group,with statistical significance(P<0.05). CONCLU-SIONS:Edaravone combined with citicoline sodium show good therapeutic efficacy in the treatment of acute cerebral infarction, can decrease the levels of oxidative stress and inflammation and promote the recovery of the neurological function and the daily liv-ing ability.
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Objective To investigate dynamic changes and clinical significance of the high-sensitive Creactive protein(hs-CRP) level in acute cerebral infarction patients with different etiological types.Methods 136 patients with acute cerebral infarction were recruited.These patients were classified into five subtypes based on Trial of Org 10172 in Acute Stroke Treatment(TOAST) criteria.Serum hs-CRP levels on the 1st,3rd,5th,7th,14th day after onset from patients and 42 healthy controls were measured with immunoturbidimetry.The neurologic impairmentscore was determined with NIHSS.Results Serum hs-CRP levels is higher on the 1th,3rd,5th,7th,14th day than that of the control group ( (4.26 ± 1.31 ),( 12.57 ± 6.29 ),( 10.23 ± 4.49 ),(7.54 ± 2.33 ),(4.25 ± 1.77) mg/Land (2.56 ± 0.86) mg/L,t = 7.89,10.26,10.99,13.55,5.97,P ＜ 0.05 ).Among 5 subtypes,serum hs-CRP was the highest in large-artery atherosclerosis group after acute ischemic stroke,and cardioembolism group was the next.Serum hs-CRP reached the highest on three or five days after disease onset and decreased slowly.High levels of hs-CRP in large-artery atherosclerosis group indicated severe neurologic functional impairment and worsen prognosis.Conclusions ACI is closely related to serum hs-CRP level,which can be used as an subjective index for severity and prognosis with the lasting,high levels of hs-CRP levels predict poor prognosis.
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OBJECTIVE:To establish an HPLC method for the determination of Tanshinone Ⅱ A in Huganning tablets.METHODS:The determination was performed by HPLC using C18 column(200 mm?4.6 mm,5 ?m) with the column temperature maintained at 25 ℃.The mobile phase consisted of methanol-water(80∶20) at a flow rate of 1.0 mL?min-1 and a UV detection wavelength of 270 nm.RESULTS: The calibration curve of Tanshinone Ⅱ A was in good linearity over the range of 4.999～44.999 ?g?mL-1(r=0.999 7) and the mean recovery was 99.07%(RSD=0.33%,n=9).CONCLUSION: The method is sensitive,accurate and reproducible,and it can be used for the quality control of Huganning tablets.
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To observe the effects of polyclonal antibodies to rat LPS binding protein on LPS induced activation of NF ?B and production of TNF ? and IL 6 in the lung. The activation of NF ?B and the contents of TNF ? and IL 6 were measured by electrophoretic mobility shift assay and ELISA respectivly. We found that both the activity of NF ?B and the levels of TNF ? and IL 6 in the lung were significantly decreased by the antibodies when used at early stage, but not at late stage after LPS challenge. These data indicated that the antibodies to LPS binding protein might have a potential value in the prevention of acute lung injury as a result of LPS challenge.