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    • Protective Effect of Astragaloside on Viral Myocarditis in Mice with CVB3

      2008, 16(3):205-208.

      Keywords:PediatricsBalb/c MiceAstragalosideCVB3 ViralMyocarditisOxygen RadicalAntioxidate
      Abstract (1357)HTML (0)PDF 4.43 M (958)Favorites

      Abstract:Aim To study protective effect and the anti-oxidize mechanism of Astragaloside on viral myocarditis in mice with CVB3. Methods Fifty Balb/c mice were randomized into five groups(n=10): normal control group,given 0.1 mL of EMEM by intraperitoneal injection,were teated with saline 0.1 mL with gavage after 30 minities of injection for 1 week;viral myocarditis Control group,inoculated intraperitoneally with 0.1 mL of 1×102 TCID50 CVB3 diluted in Eagles minimal essential medium(EMEM) solution were given saline 0.1 mL with gavage after 30 minities of injection for 1 week;Astragaloside lowdose intervention group,middle-dose intervention group and high-dose intervention group,inoculated intraperitoneally with 0.1 mL of 1×102 TCID50 CVB3 diluted in Eagles minimal essential medium(EMEM) were treated with 1%,3% and 9% astragaloside 0.07,0.2 and 0.6 g/(kg·d),respectively] 0.1 mL solution after 30 minetes of injection,respectively with gavage for 1 week.Survival number,score of pathological changes,GSH-PX,CAT,SOD and CuZn-SOD-mRNA of myocardium were detected. Results The survival number was significantly improved in Balb/c mice treated with high dose astragaloside group than that in viral myocarditis control group(P<0.01).Heart function was better in high-dose intervention group than in the viral myocarditis control group,the activity of GSH-PX,CAT,SOD and CuZnSOD -mRNA levels was enhanced and heart function was improved in group high dose astragaloside group than in viral myocarditis control group(P<0.01). Conclusion The results showed that astragaloside can provide protection against viral myocarditis.This protective effect of astragaloside may be related to the maintenance of the antioxidant status of the heart in improving myocardial antioxidant enzymes activity .

    • Protective Role of Unsaturated Fatty Acid of Actinidia Chinesis Planch Seed Oil on Adriamycin-Induced Myocardium Injury in Rat and mechanism of its Action

      2006, 14(1):25-28.

      Keywords:Actinidia ChinesisPlanch seed OilUnsaturated Fatty Acidα-Linolenic AcidMyocardium InjuryOxygen RadicalAdriamycin
      Abstract (1139)HTML (0)PDF 4.45 M (1025)Favorites

      Abstract:Aim To observe the protective role of unsaturated fatty acid of actinidia chinesis planch seed oil(UFAACPSO) on adriamycin-induced myocardium injury in rat and clarify the mechanism of its action. Methods Forty SD rat were randomly divided into four groups:Control group(physical salts filled into stomach and injected into pleural),ADR group(physical salts filled into stomach and adriamycin injected into pleural),ADR+Lg group (low concentration UFAACPSO filled into stomach and adriamycin injected into pleural),ADR+Hg group(high concentration UFAACPSO filled into stomach and adriamycin injected into pleural).The death rate was calculated.Creatine kinase isoenzyme MB(CK-MB),glutathione peroxidase(GSH-Px),catalase(CAT),copper-zinc-superoxide dismutase(Cu-Zn-SOD) were detected.The expression level of Cu-ZnSOD protain and mRNA were detected by immunhistochemical method and semi-quantitative reverse transcriptase-polymerase chain reaction(RT-PCR). Results The change rate of heart rate of ADR+Hg group was obviously lower than ADR group(p<0.05),the activity of Cu-Zn-SOD,CAT and GSH-Px of ADR+Hg group were obviously than higher than ADR group(p<0.05),serum CK-MB concentration of ADR+Hg group was obviously lower than ADR group(p<0.01),Cu-Zn-SOD protein,mRNA expression were up-regulated remarkably in ADR+Hg group(p<0.05),and the death rate was reduced in ADR+Hg group.But no significantly difference was not found between ADR group and ADR+Lg group and adriamycin group. Conclusion UFAACPSO could significantly decrease adriamycin-induced myocardium injury in rat,the mechanism of its action may related to its activity of reducing oxygen radical and inhibiting oxidative stress.

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