Inhibition of Palmitic Acid-induced Cardiomyocyte Apoptosis by Oridonin and Its Mechanism

OBJECTIVE To investigate the effect of oridonin(Ori) on the apoptosis of H9C2 cells induced by palmitic acid(PA) and its mechanism.

METHODS  H9C2 cells were treated with PA for 24 h. Cell viability was detected by MTT assay. The protein expression levels of Cleaved Caspase 3, Nrf2, NQO1 and HO1 were detected by Western blotting. The quantity of superoxide anions was measured using a DHE fluorescence probe. Cardiomyocyte apoptosis was detected by TUNEL.

RESULTS When H9C2 cells were treated with 200 μmol·L⁻¹ PA for 24 h, compared with the control group, cell viability was significantly decreased; the protein expression level of Cleaved Caspase 3 and positive cardiomyocyte apoptosis(red) were significantly increased; the number of superoxide anions was significantly increased, and the protein expression levels of Nrf2, NQO1 and HO1 were significantly down-regulated(P<0.05). After Ori treatment, compared with PA group, the cell viability was significantly increased; the protein expression level of Cleaved Caspase 3 and the positive cardiomyocyte apoptosis(red) were significantly decreased; the number of superoxide anions was significantly decreased; and the protein expression levels of Nrf2, NQO1 and HO1 were significantly increased(P<0.05). However, Nrf2 inhibitor treatment reversed the above changes.

CONCLUSION Ori alleviates PA-induced cardiomyocyte apoptosis by activating the Nrf2/ARE signaling pathway.