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作 者:黄琦[1] 邓雯雯[2] 许家鸾[2] 王京霞[2] 叶程程[2]
机构地区:[1]浙江中医药大学附属第一医院,杭州310006 [2]浙江中医药大学,杭州310053
出 处:《中药新药与临床药理》2012年第5期500-504,共5页Traditional Chinese Drug Research and Clinical Pharmacology
摘 要: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 in-vitro effect of total saponins of Radix Ginseng(TSRG) on the apoptosis of human umbilical vein endothelial cells (HUVEC) induced by intermittent high glucose and activity of superoxide dismutase(SOD) and content of malondialdehyde(MDA), to explore their possible protective mechanism. Methods After establishing the intermittent high glucose injury model, we detected HUVEC injuries induced by the intermittent high glucose with MTT, oberved HUVEC morphological changes in each experimental group, tested the effects of TSRG on HUVEC apoptosis by flow cytometry and measured the expression of SOD and MAD in culture supernatant of each experimental group. Results (1)Normal cells looked like paving stones and had clear boundary, but the cells in the experimental groups had different degrees of injury, while the cells morphology in TSRG group was improved compared with the than intermittent high glucose model group. (2)Compared with the blank control group, the rate of HU- VEC apoptosis induced by intermittent high glucose was high, MDA expression increased, and the activity of SOD decreased obviously, the differences being significant (P 〈 0.001 ). (3) After treating with different concentrations of TSRG, HUVEC apoptosis rate was decreased, the activity of SOD was increased and MDA was decreased, the differ- ences being significant as compared with intermittent high glucose group(P 〈 0.05). Conclusion TSRG could significantly inhibit the HUVEC apoptosis induced by intermittent high glucose, and induce the increase of SOD activity and the decrease of MDA content in cell supernatant, which shows protective effect on HUVEC injury induced by intermitten high glucose
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