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目的:探讨人参皂苷Rb1对间歇性高糖培养条件下雪旺细胞氧化应激的影响。方法:无菌剥取新生Sprague-Dawley乳鼠坐骨神经,体外制备雪旺细胞,分为对照组(培养液葡萄糖浓度为5.6 mmol/L,Con组)、间歇性高糖组(培养液葡萄糖浓度为5.6 mmol/L和50 mmol/L每8 h交替,IHG组)、干预组(在间歇性高糖基础上加入100μmol/L人参皂苷Rb1,IHG+Rb1组)分别培养48 h。MTT法检测细胞活性,流式细胞仪检测细胞内ROS,提取DNA后采用ELISA法检测8-OHd G。结果:IHG组雪旺细胞活性明显下降,是Con组的70.1%(P<0.05);ROS、8-OHd G水平均明显高于Con组,分别是Con组的2.86倍、3.24倍(P<0.01)。人参皂苷Rb1干预可以改善间歇性高糖导致的细胞活性下降,IHG+Rb1组细胞活性增加到IHG组的1.27倍(P<0.05);人参皂苷Rb1抑制了间歇性高糖引起的ROS、8-OHd G升高,IHG+Rb1组ROS、8-OHd G水平分别较IHG组下降了36.7%和32.7%(P<0.05)。结论:间歇性高糖可诱导雪旺细胞产生氧化应激造成神经细胞损伤,人参皂苷Rb1能够减轻上述反应,具有一定的神经保护作用。
Objective: To investigate the effects of ginsenoside Rb1 on oxidative stress in Schwann cells under intermittent high glucose conditions. METHODS: Schwann cells were isolated from aseptic newborn Sprague-Dawley rats and cultured in vitro. The rats were divided into control group (glucose concentration 5.6 mmol / L, Con group), intermittent high glucose group (glucose concentration 5.6 mmol / L and 50 mmol / L alternation every 8 h, IHG group), and intervention group (100 μmol / L ginsenoside Rb1, IHG + Rb1 group on intermittent high glucose) were cultured for 48 h. Cell viability was measured by MTT assay. ROS was detected by flow cytometry. DNA was extracted by enzyme-linked immunosorbent assay (ELISA) for 8-OHdG. Results: The activity of Schwann cells in IHG group was significantly lower than that in Con group (70.1%, P <0.05), while the levels of ROS and 8-OHd G in Con group were 2.86 and 3.24 times higher than those in Con group 0.01). Ginsenoside Rb1 could improve cell activity induced by intermittent high glucose, cell viability in IHG + Rb1 group was 1.27 times higher than IHG group (P <0.05); Ginsenoside Rb1 inhibited the intermittent high glucose-induced ROS, 8- OHd G, the level of ROS and 8-OHd G in IHG + Rb1 group decreased by 36.7% and 32.7% respectively compared with IHG group (P <0.05). CONCLUSION: Intermittent high glucose can induce oxidative stress in Schwann cells and cause neuronal damage. Ginsenoside Rb1 can alleviate the above reaction and has certain neuroprotective effects.