目的:研究红景天苷(对-羟基苯乙基-B-葡萄糖,p-hydroxyphenethyl-b-D-glucoside,Salidroside,SAL)对1-甲基-4-苯基吡啶离子(1-methy-4-phenylpyridinium,MPP+)诱导PCI2细胞凋亡的影响及其可能机制。方法:4-甲基偶氮唑蓝(MTT)检测PCI2细胞活性;Hochest 33258染色,观察细胞凋亡的变化;Western blot检测核因子2相关因子2(nuclearfactor-erythroid 2 p45,related factor2,Nrf2)蛋白的表达情况。结果:MPP+(500μmol/L)作用于PCI2细胞24h后,与正常组比较,细胞存活率降低(53.3%±3.4%,P〈0.01);细胞内染色质固缩,呈致密浓染。SAL(10,100μmol/L)预处理24h后,细胞存活率增加(60.8±1.9)%和(87.1土1.8)%(P〈0.01);细胞核固缩明显减少,且具有剂量依赖性关系。此外,MPP+可使PCI2细胞中Nrf2蛋白表达减少,而SAL预处理后,PCI2细胞中Nrt2蛋白表达水平明显升高。结论:SAL对MPP+诱导的PCI2细胞凋亡具有浓度依赖性的抑制作用,其作用机制可能与促进Nrf2蛋白的激活有关。
Objective: To explore the protective effect of p-hydroxyphenethyl-b- D-glucoside (Salidroside) on 1-methy- 4-phenylpyridinium( MPP~) induced apoptosis in PC12 cells and its possible mechanism. Methods: The cell viability was measured by 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyhetrazolium bromide (MTF). The morphological change of PC12 cells was observed by Hoechst 33258 staining. The expression level of nuclear factor-erythroid 2 p45, related factor 2 (Nrt2) protein was detected by Western blot. Results: Compared with the control group, the ratio of cell survival de- creased 53.3 + 3.4% (P 〈 0.01 ); eyto-ehromatin concentration; nucleus showing strong staining after MPP+ treatment with PC12 cells for 24 h. The cell viability was increased to 60.8 ± 1.9%, 87.1 ± 1.8% (P 〈0.01 ) respectively after exposure with 10,100 μmol/L SAL. Cyto-chromatin concentration reduced and showed the relation between quantity and results. Furthermore, MPP +decreased the expression level of Nrf2 protein in the cytoplasm of PC12 cells. But compared with MPP+ treatment group, the expression level of Nrf2 protein in the cytoplasm of PC12 cells was increased after SAL pretreatment. Conclusion: SAL plays a possible neuroprotective role in MPP + induced apoptosis of PC12 cells by a con-centration-dependent manner, and the mechanism of the effects of SAL may be involved in facilitating Nrf2 activation.