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作 者:孙菁[1] 孟凡山[1] 陈威[1] 计达[1] 沈洪[1]
机构地区:[1]中国人民解放军总医院急诊科,北京市100853
出 处:《中国全科医学》2011年第5期497-499,502,共4页Chinese General Practice
基 金:国家高技术研究发展计划(863)项目(2002AA2Z3321)
摘 要:目的探讨山莨菪碱(anisodamine,Ani)对缺氧复氧损伤血管内皮细胞凋亡的影响。方法采用人脐静脉内皮细胞缺氧复氧方法观察血管内皮细胞凋亡的变化,实验分5组:对照组、生理盐水组、肾上腺素组、Ani组、肾上腺素+Ani组。采用流式细胞术检测细胞凋亡,采用RT-PCR法检测血管内皮细胞B细胞淋巴瘤/白血病-2基因(Bcl-2)mRNA表达水平。结果 5组血管内皮细胞复氧12 h、24 h的细胞凋亡率比较,差异均有统计学意义(P<0.05)。其中生理盐水组复氧12 h、24 h细胞凋亡率与肾上腺素组、Ani组、肾上腺素+Ani组比较,差异均有统计学意义(P<0.05)。肾上腺素组与Ani组复氧12 h、24 h细胞凋亡率比较,差异均无统计学意义(P>0.05);而这两组与肾上腺素+Ani组复氧12 h、24 h的细胞凋亡率比较,差异均有统计学意义(P<0.05)。复氧12 h、24 h后5组的Bcl-2 mRNA表达水平比较,差异均有统计学意义(P<0.05)。肾上腺素+Ani组Bcl-2 mRNA表达水平明显升高,差异有统计学意义(P<0.05)。结论 Ani可以降低缺氧血管内皮细胞的凋亡。Ani干预缺氧所致血管内皮细胞损害,可能与影响Bcl-2 mRNA表达有关。Objective To explore the influence of anisodamine on human umbilical vein endothelial cells′(HUVECs) apoptosis induced by hypoxia and reoxygenation.Methods The HUVECs were divided into groups control(group A),hypoxia-reoxygenation 0.9% saline(group B),hypoxia-reoxygenation epinephrine(group C),hypoxia-reoxygenation Ani(group D),hypoxia-reoxygenation epinephrine plus Ani(group E).The cell apoptoses were detected by fluorescence flow cytometry,the gene expression of Bcl-2 by reverse transcription-polymerase chain reaction(RT-PCR).Results There was significant difference in apoptotic indexes(AI) of HUVECs at hours 12,24 of reoxygenation between 5 groups(P0.05),group B were significantly different from groups C,D,E(P0.05),group C not from group D(P0.05),but groups C,D from group E(P0.05).There was significant difference in Bcl-2mRNA level between 5 groups at hours 12,24 of reoxygenation(P0.05),and Bcl-2mRNA expression increased more significantly in group Ethan in other groups(P0.05).Conclusion Ani can reduce apoptosis of HUNVECs after hypoxia-reoxygenation.Ani protects the function of endothelia cells after hypoxia-reoxygenation by influencing the mRNA expression of Bcl-2.
分 类 号:R322.74[医药卫生—人体解剖和组织胚胎学]
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