| 陶丽珍1 栗艳2 李晓冰1 李晓峰1 孙欣1 陈建宗1.二苯乙烯苷通过抑制NF-κB的激活减轻MPP+诱导
的PC12细胞凋亡[J].,2011,11(4):668-671 |
| 二苯乙烯苷通过抑制NF-κB的激活减轻MPP+诱导
的PC12细胞凋亡 |
| Effect of 2，3，5，4'-tetrahydroxystibene-2-o-β-D-glucoside in mitigationof MPP+-induced Apoptosis of PC12 Cells |
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| DOI： |
| 中文关键词: 二苯乙烯苷 MPP+ PC12细胞 凋亡 NF-κB |
| 英文关键词: tetrahydroxystilbene glucoside MPP+ PC12 cells apoptosis NF-κB |
| 基金项目:国家自然科学基金（30772743） |
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| 中文摘要: |
| 目的：探讨2，3，5，4'- 四羟基二苯乙烯-2-o-β-D- 葡萄糖苷(2，3，5，4'-tetrahydroxystibene-2-o-β-D-glucoside,TSG)对1- 甲基
-4- 苯基吡啶离子(1-methy-4-phenylpyridinium，MPP+)诱导PC12 细胞凋亡的影响及其可能机制。方法：四甲基偶氮唑蓝(MTT)比
色试验检测PC12细胞活性；Hoechst33258 染色法测定细胞凋亡；Western blotting检测NF-κB(P65)和IκBα蛋白的表达。结果：
MPP+(300μmol/L)作用于PC12细胞24h后，与正常对照组比较，细胞存活率降低(53.3±3.4%)(P<0.01)；细胞染色质固缩，细胞核
呈致密浓染。TSG(1,5,10μmol/L)预处理24h后，细胞存活率增加(60.8±1.9%),(70.1±1.8%)(P<0.01),(81.2±1.9%)(P<0.01)；细胞核
凝聚明显减少，且具有量一效关系。另外，MPP+ 可使PC12 细胞核中NF-κB (P65)蛋白表达升高,细胞浆中IκBα 蛋白表达降
低；与MPP+处理组细胞相比，TSG预处理后, PC12细胞核中高表达的NF-κB (P65)蛋白水平明显降低，细胞浆中低表达的IκBα
蛋白水平升高。结论：TSG对MPP+ 诱导的PC12 细胞凋亡具有浓度依赖性的抑制作用，其作用机制可能与抑制NF-κB 的激活
有关。 |
| 英文摘要: |
| Objective: To explore the protective effect of TSG on MPP+ induced PC12 cells apoptosis. Methods: The PC12 cells
viability was measured by 3-[4,5-dimethylthiazol-2-y1]-2, 5-diphenyhetrazolium bromide(MTT).The morphological change of PC12 cells
was observed by Hoechst 333258 staining. The expression level of NF-κB (P65) and IκBα protein was detected by Western blotting.
Results: Compared with the control group, the ratio of cell survival decreased (53.3±3.4%)(P<0.01); cyto-chromatin concentration; nucleus
showing strong staining after MPP+ treatment with PC12 cells for 24h. The ratio of cell survival increased (60.8±1.9%),(70.1±
1.8%)(P<0.01),(81.2±1.9%)(P<0.01)after TSG (1, 5,10μmol/L) pretreatment with PC12 cells for 24h; cyto-chromatin concentration reduced
and show the relation between quantity and result. Moreover, MPP+ is able to increase the expression level of NF-κB(P65)protein
in the nucleus，decrease the expression level of IκBα protein in the cytoplasm of PC12 cells. The high expression level of NF-κB(P65)
protein in the nucleus is decreased and the low expression level of IκBα protein in the cytoplasm of PC12 cells is increased after TSG
pretreatment with PC12 cells, compared with MPP+ treatment group. Conclusion: TSG plays a possible neuroprotective role in MPP+-induced
apoptosis of PC12 cells by a concentration-dependent manner, and the mechanism of the effects of TSG may be involved in inhibiting
NF-κB activation. |
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