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孟娜娜, 李厚忠, 温以杰, 刘洁婷, 左魁阳, 李鲁新, 金秀东, 张羽飞. 柚皮苷对H2O2诱导H9c2心肌细胞损伤保护作用[J]. 中国公共卫生, 2018, 34(3): 377-380. DOI: 10.11847/zgggws1116975
引用本文: 孟娜娜, 李厚忠, 温以杰, 刘洁婷, 左魁阳, 李鲁新, 金秀东, 张羽飞. 柚皮苷对H2O2诱导H9c2心肌细胞损伤保护作用[J]. 中国公共卫生, 2018, 34(3): 377-380. DOI: 10.11847/zgggws1116975
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Na-na MENG, Hou-zhong LI, Yi-jie WEN, . Protective effect of naringin on H9c2 myocardial cell injury induced by H2O2[J]. Chinese Journal of Public Health, 2018, 34(3): 377-380. DOI: 10.11847/zgggws1116975
Citation: Na-na MENG, Hou-zhong LI, Yi-jie WEN, . Protective effect of naringin on H9c2 myocardial cell injury induced by H2O2[J]. Chinese Journal of Public Health, 2018, 34(3): 377-380. DOI: 10.11847/zgggws1116975
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柚皮苷对H2O2诱导H9c2心肌细胞损伤保护作用

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

    摘要
  • 摘要:
      目的  探讨柚皮苷对H2O2诱导的H9c2心肌细胞凋亡的保护作用及机制。
      方法  体外培养H9c2心肌细胞，用H2O2诱导建立细胞凋亡模型。实验设对照组、模型组、柚皮苷低、中、高剂量组（10、20、40 μmol/L），噻唑蓝法检测细胞活力并用显微镜观察各组细胞形态；原位末端标记法检测H9c2心肌细胞凋亡情况；RT-PCR及Western blot法检测凋亡相关因子Bcl-2、Bax、caspase-3 mRNA及蛋白表达。
      结果  与对照组比较，模型组细胞凋亡率（17.2 ± 2.1）%明显升高（P < 0.01）；与模型组比较，10、20、40 μmol/L柚皮苷组细胞凋亡率分别为（10.7 ± 1.9）%、（5.7 ± 1.2）%、（6.4 ± 1.5）%均下降（均P < 0.05）。与对照组比较，模型组H9c2心肌细胞Bcl-2蛋白表达水平（0.76 ± 0.16）明显下调，Bax、caspase-3蛋白表达水平分别为（5.42 ± 0.52）、（1.09 ± 0.11）均上调（均P < 0.01）；与模型组比较，10、20、40 μmol/L柚皮苷组H9c2心肌细胞Bcl-2蛋白表达水平分别为（1.37 ± 0.11）、（1.65 ± 0.09）、（1.65 ± 0.15）均上调，Bax、caspase-3蛋白表达水平分别为（2.78 ± 0.55）、（3.43 ± 0.15）、（2.69 ± 0.26）和（0.59 ± 0.08）、（0.77 ± 0.06）、（0.82 ± 0.05）均下调（均P < 0.05）。
      结论  柚皮苷对H2O2诱导的H9c2心肌细胞损伤具有一定保护作用，其机制可能与其对凋亡信号途径的抑制作用有关。

     

    Abstract:
      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.

     

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