Protective effect of naringin on H9c2 myocardial cell injury induced by H₂O₂

  Objective  To examine the protective effect and mechanism of naringin on H₂O₂-induced apoptosis of H9c2 myocardial cells.

  Methods  H9c2 myocardial cells were cultured in vitro and a H9c2 myocardial cell apoptosis model was induced with hydrogen peroxide (H₂O₂). Five H9c2 myocardial cell groups were established: a control, model, low-, moderate-, and high-dose (10, 20, and 40 μmol/L) naringin pretreatment group. Cell viability was detected with 3- (4, 5-dimethyl-2-thiazolyl) -2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay and cell morphology was observed with microscope. The apoptosis of H9c2 myocardial cells was detected with terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) method. The expressions of B cell lymphoma 2 (Bcl-2), BCL2-associated X protein (Bax), caspase-3 mRNA and protein were detected with real-time reverse transcription PCR (RT-PCR) and Western blot.

  Results  Compared with that of the control group, the apoptotic rate (17.2 ± 2.%) of the model group was significantly higher (P < 0.01); compared with that the model group, the apoptotic rate of low-, moderate-, and high-dose naringin pretreatment group were significantly decreased (10.7 ± 1.9%, 5.7 ± 1.2%, and 6.4 ± 1.5%) (all P < 0.05). The Bcl-2 protein expression (0.76 ± 0.16) in H9c2 cardiomyocytes of the model group was significantly lower and the protein expressions of Bax and caspase-3 were significantly increased compared to those of the control group (all P < 0.01). The protein expressions of Bcl-2 (1.37 ± 0.11, 1.65 ± 0.09, and1.65 ± 0.15) in H9c2 myocardial cells of low-, moderate-, and high-dose naringin pretreatment group were significantly increased; while those of Bax (2.78 ± 0.55, 3.43 ± 0.15, and 2.69 ± 0.26) and caspase-3 (0.59 ± 0.08, 0.77 ± 0.06, and 0.82 ± 0.05) were significantly decreased compared to those of the control group (all P < 0.05).

  Conclusion  Naringin could inhibit apoptosis of H9c2 myocardial cells induced by H₂O₂, which may be related to its inhibitory effect on the apoptotic signaling pathway.