Volume 16 Issue 1
Jul.  2022
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DING Jie, DOU Peng-fei. Effect of epigallocatechin gallate on daunorubicin-induced cardiotoxicity in mice[J]. Chinese Journal of General Practice, 2018, 16(1): 26-29. doi: 10.16766/j.cnki.issn.1674-4152.000007
Citation: DING Jie, DOU Peng-fei. Effect of epigallocatechin gallate on daunorubicin-induced cardiotoxicity in mice[J]. Chinese Journal of General Practice, 2018, 16(1): 26-29. doi: 10.16766/j.cnki.issn.1674-4152.000007

Effect of epigallocatechin gallate on daunorubicin-induced cardiotoxicity in mice

doi: 10.16766/j.cnki.issn.1674-4152.000007
  • Received Date: 2017-04-06
  • Objective To observe the prevention effect of Fructose-1, 6-diphosphate (FDP) and Epigallocatechin gallate (EGCG) against the daunorubicin-induced myocardial injury in mice. Methods The Kunming mice were randomly divided into normal control group, model group, positive control group (FDP group), drug intervention group (EGCG group), with 20 mice in each group. The mice in the FDP group and EGCG group were given FDP and EGCG (40 mg/kg) by intragastric administration, and the mice in the normal control group and model group were given equal volume of normal saline. One week later, the mice in the model group, FDP group and EGCG group were given daunorubicin (20 mg/kg) by intraperitoneal injection, while in the control group were given normal saline. Forty-eight hours after daunorubicin was administrated, All the mice were taken the blood to test the levels of myocardial enzyme (CK-MB, AST, -HBDH). The experimental data were analyzed by using SPSS 19.0. Results The survival rate of normal control group was 100%, which was higher than that of the model group (60%); however, the level of myocardial enzyme in the model group was higher than that in the control group (P<0.01). The survival rate (90%) of both FDP group and EGCG group was higher than that of the model group, and the level of myocardial enzyme was decreased (P<0.01), especially in the EGCG group (P<0.05). Conclusion FDP and EGCG can depress the cardiotoxicity of daunorubicin in mice, especially the latter.

     

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