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Effect of Evodiamine on Hypoxia Induced Cardiomyocytes Injury / 中国药师
China Pharmacist ; (12): 193-197, 2018.
Article in Chinese | WPRIM | ID: wpr-705487
ABSTRACT

Objective:

To investigate the protective effect of evodiamine on cardiomyocytes hypoxia injury.

Methods:

H9c2 myo-cardial cells were exposed to hypoxia for 24 h to induce myocardial cell injury model. The cells were pretreated with different concentra-tions of evodiamine for 12 h. The cardiomyoctes viability was detected by CCK-8 assay. The transcription of inflammatory cytokines was detected by RT-PCR. The cardiomyocyte apoptosis was detected with Tunel staining. The alteration of signal pathway was detected by immunoblotting.

Results:

Four concentrations of evodiamine did not affect the activity of cardiomyocytes in the basal condition (P>0.05). After 24-hour hypoxia,the viability of cardiomyocytes decreased significantly when compared with that in the control group with significant difference (P<0.05) among 1,5 and 10 μmol·L-1evodia in a dose-dependent manner. The transcription of pro-inflam-matory cytokines(TNF-α,IL-1 and IL-6) significantly increased and the cells apoptosis increased. Evodiamine pretreatment increased the cell viability after hypoxia injury, reduced the transcription of inflammatory cytokines and reduced the number of apoptotic cells when compared with that in the control group with significant differences(P<0.05) between 1 μmol·L-1and 10 μmol·L-1evodia. The results of western blot showed that evodiamine activated AMPKα and AKT, inhibited the activity of NF- kappa B, and compared with the control group,there were significant differences(P<0.05) between 1 μmol·L-1and 10 μmol·L-1of evodia.

Conclusion:

Evodiamine can protect cardiomyocytes from hypoxia injury and may become a new anti-myocardial ischemia drug.

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: China Pharmacist Year: 2018 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: China Pharmacist Year: 2018 Type: Article