枸杞多糖对缺氧损伤PC12细胞的保护作用

Protective effects of Lycium barbarum polysacchrides on anoxia injury in cultured PC12 cells

目的观察枸杞多糖对化学缺氧损伤大鼠肾上腺嗜铬细胞瘤株PC12细胞的保护作用,并探讨可能的作用机制。方法建立氯化钴(CoCl_2)诱导PC12细胞化学缺氧损伤模型,通过测定不同浓度枸杞多糖处理前后细胞活力、细胞凋亡率、线粒体膜电位及细胞内Ca^(2+)含量的变化,探讨枸杞多糖对缺氧损伤细胞的保护作用。结果对照组、缺氧模型组和100 mg/L枸杞多糖组的细胞存活率、细胞凋亡率和细胞内Ca^(2+)含量分别为(100.00±4.23)%、(48.54±5.59)%和(83.11±6.67)%,0.7%、76.8%和11.5%,(24.2±3.94)、(75.3±6.82)和(34.3±3.05),100 mg/L枸杞多糖组的细胞存活率明显高于缺氧模型组,而细胞凋亡率和细胞内Ca^(2+)含量均低于缺氧模型组,差异均有统计学意义(P<0.05)。缺氧模型组PC12线粒体膜电位显著降低,为对照组的(43.2±2.46)%,100 mg/L的枸杞多糖组为(73.3±2.85)%,明显上升,差异有统计学意义(P<0.05)。结论缺氧模型可抑制PC12细胞增殖并诱导细胞凋亡,枸杞多糖对缺氧损伤PC12细胞具有明显的保护作用,可能与增加细胞线粒体膜电位及降低细胞内Ca^(2+)含量有关。

Objective To investigate the protective effect of Lycium barbarum polysacchrides（LBP） on anoxia injury incultured PC12 cells, and discuss the mechanism. Methods The hypoxia-induced nerve cell injury model was established.The protective effect of LBP on the model was evaluated by the celluar survival rate, cell apoptosis assay, the concentration ofintracellular calcium, and mitochondrial membrane potential. Results The cell survival rate, apoptosis rate and the content ofintracellular Ca^2＋ of model control group, hypoxia group and 100 mg/L LBP group were（100.00±4.23）%,（48.54±5.59）% and（83.11＋6.67） %, 0.7%, 76.8% and 11.5%,（24.2±3.94）,（75.3±6.82） and（34.3±3.05）, respectively. And the cell survival rate of100 mg/L LBP group was obviously higher than that of hypoxia model group, the apoptosis rate and the content of intracellularCa^2＋were lower than hypoxia model group, the differences were statistically significant（P〈0.05）. The mitochondrial membranepotential of PC12 was significantly reduced in the hypoxia model group, for（43.2±2.46）% of the control group, and（73.3±2.85）% of 100 mg/L LBP group, significantly increased, and the difference was statistically significant（P〈0.05）.Conclusion The hypoxia model could induce the apoptosis of PC12 cells and LBP has a remarkably protective effect onanoxia injury in cultured PC12 cells, and the effects of protection may be associated with the increase of the mitochondrialmembrane potential and inhibition of the concentration of intracellular calcium.