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首页> 外文期刊>Journal of Behavioral and Brain Science >Isoflavone Attenuates the Nuclear Transcription Factor Kappa B (NF-&i&κ&/i&B) Activation on MPP&sup&+&/sup&-Induced Apoptosis of PC12 Cells
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Isoflavone Attenuates the Nuclear Transcription Factor Kappa B (NF-&i&κ&/i&B) Activation on MPP&sup&+&/sup&-Induced Apoptosis of PC12 Cells

机译：异黄酮在MPP +上衰减核转录因子Kappa B（nF- I＆κ＆＆ / i＆ b）活化。 - -c1 / sup＆诱导pC12细胞的凋亡

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Objective: To explore the underlying molecular mechanisms of cellular response to the challenge by 1-methyl-4-phenylpyridinium (MPP ~(+) )-induced apoptosis of PC12 cells, an in vitro cell model for Parkinson’s disease, and the effect of NF-κ B activation on the protection of Parkinson’s disease by Isoflavone (I). Methods: PC12 cells were used to establish the cell model of Parkinson’s disease, and are divided into five groups: control group; MPP ~(+) group; I (Isoflavone) + MPP ~(+) group; I group; SN-50 + MPP ~(+) group. The content of NF-κ B in PC12 cells was determined by immunocytochemistry; The viability of PC12 cells after treated with cell-permeable NF-κ B inhibitor SN-50 and cell viability were measured by MTT assay; the expression levels of NF-κ B p65 in cytoplasm and nuclear fractions were evaluated by western blot analysis; the mRNA expression of NF-κ B p65 was analyzed by in situ hybridization (ISH). Results: Compared with the control group, the protein of NF-κ B p65 both in cytoplasm and in nuclei was significantly higher than in I + MPP ~(+) and MPP ~(+) groups; similarly, the mRNA expression level of NF-κ B p65 gene was also significantly higher; moreover, the protein expression of NF-κ B p65 was much lower in I group (P < 0.05). In addition, compared with the MPP ~(+) group, the protein of NF-κ B p65 was significantly lower in I + MPP ~(+) group, the mRNA expression level of NF-κ B p65 gene was also significantly lower, and the protein expression level of NF-κ B p65 was much lower in I + MPP ~(+) group (P < 0.05); however, there was no significant difference between control group and I + MPP ~(+) group ( P > 0.05). Conclusion: NF-κ B activation is essential to MPP ~(+) -induced apoptosis in PC12 cells; but Isoflavone can inhibit the cell damage to some extent to execute its protective function, which may be involved in nigral neurodegeneration in patients with Parkinson’s disease.
机译：目的：探讨1-甲基-4-苯基吡啶（MPP〜（+））诱导PC12细胞凋亡的细胞反应的潜在分子机制，帕金森病的体外细胞模型，以及NF的影响 - κBseSoflavone（i）对帕金森病的激活。方法：使用PC12细胞来建立帕金森病的细胞模型，分为5组：对照组; MPP〜（+）组; I（异黄酮）+ MPP〜（+）组;我组; SN-50 + MPP〜（+）组。通过免疫细胞化学确定PC12细胞中NF- κB的含量;通过MTT测定法测定了用细胞可渗透的NF- 0.05）。结论：NF- κB活化对于MPP〜（+） - 诱导PC12细胞的细胞凋亡至关重要;但异黄酮可以在一定程度上抑制细胞损伤，以执行其保护功能，这可能参与帕金森病患者的Nigral神经变性。

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