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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 observe the protective effect of Lycium barbarum polysaccharides on adrenal pheochromocytoma PC12 cells induced by chemical hypoxia in rats and its possible mechanism. Methods CoCl2 was used to induce chemical hypoxic injury in PC12 cells. The changes of cell viability, apoptosis rate, mitochondrial membrane potential and intracellular Ca2 + content before and after treatment with LBP were determined Protective effects of lycium barbarum polysaccharides on hypoxic injury cells. Results The cell viability, apoptosis rate and intracellular Ca2 + content in control group, hypoxia model group and 100 mg / L LB group were (100.00 ± 4.23)% and (48.54 ± 5.59)%, respectively And (83.11 ± 6.67)%, 0.7%, 76.8% and 11.5%, (24.2 ± 3.94) and (75.3 ± 6.82) and (34.3 ± 3.05) and 100 mg / L respectively. Oxygen model group, while the apoptosis rate and intracellular Ca2 + content were lower than the hypoxia model group, the difference was statistically significant (P <0.05). The mitochondrial membrane potential of PC12 in hypoxia model group was significantly lower than that in control group (43.2 ± 2.46)% and (73.3 ± 2.85)% in 100 mg / L LB group, with significant difference ). Conclusions The hypoxia model can inhibit the proliferation of PC12 cells and induce apoptosis. LBP has a significant protective effect on PC12 cells injured by hypoxia, which may be related to the increase of mitochondrial membrane potential and the decrease of intracellular Ca2 + content.