论文部分内容阅读
目的观察人参总皂苷(TSPG)在体外培养的波动性高糖环境下对人脐静脉内皮细胞(HUVEC)凋亡及超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量的影响,探讨其可能的保护性干预作用。方法参考文献报道,选用HUVEC进行体外培养,建立波动性高糖损伤模型,用MTT法检测波动性高糖对HUVEC的损伤情况;观察各实验组HUVEC形态学变化;流式细胞术检测TSPG对HUVEC凋亡的影响;测定各实验组培养上清液中SOD、MDA水平。结果 (1)空白对照组细胞呈形态较规则的铺路石样且边界清楚,其他实验组细胞生长均有不同程度的损伤,但加TSPG组细胞形态变化明显优于波动性高糖组;(2)波动性高糖可诱导HUVEC产生凋亡,凋亡率明显高于空白对照组,MDA含量升高,而SOD活性则明显下降,两组比较,差异具有显著性意义(P<0.001);(3)人参总皂苷组的HUVEC凋亡率下降,SOD活性上升,MDA含量下降,与模型组比较,均有显著性差异(P<0.05)。结论 TSPG可明显抑制波动性高糖所致的HUVEC凋亡,可使细胞上清液中SOD活性增加,MDA含量降低,从而对波动性高糖所致的HUVEC损伤表现出一定的保护作用。
Objective To observe the effects of total ginsenoside (TSPG) on the apoptosis and the activity of superoxide dismutase (SOD) and malondialdehyde (MDA) in human umbilical vein endothelial cells (HUVECs) To explore its possible role of protective intervention. Methods References HUVEC were selected for in vitro culture to establish a model of fluctuating high glucose injury, MTT assay was used to detect the damage of HUVEC induced by high glucose. The morphological changes of HUVEC in each experimental group were observed. Flow cytometry was used to detect the effect of TSPG on HUVEC Apoptosis. The levels of SOD and MDA in the culture supernatant of each experimental group were determined. Results (1) The cells in blank control group showed a regular morphology of paving stones with clear boundary. The growth of cells in other experimental groups all had different degrees of damage. However, the morphological changes of cells in TSPG group were significantly better than those in hyperglycemic group (2) ) Fluctuating high glucose could induce apoptosis of HUVEC, the apoptosis rate was significantly higher than that of the blank control group, the content of MDA increased, but the activity of SOD decreased obviously. There was significant difference between the two groups (P <0.001); ( 3) The apoptosis rate of HUVEC in ginseng total saponin group decreased, SOD activity increased, MDA content decreased, compared with the model group, there was a significant difference (P <0.05). Conclusion TSPG can significantly inhibit the apoptosis of HUVEC induced by fluctuating high glucose, increase the activity of SOD and decrease the content of MDA in the supernatant of the cells, and thus protect the HUVEC induced by high glucose.