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    朱晔斌, 朱晔荣. 异常血流动力对HUVEC胆固醇代谢的影响及其致AS的机制[J]. 徐州医科大学学报, 2022, 42(3): 163-169. DOI: 10.3969/j.issn.2096-3882.2022.03.002
    引用本文: 朱晔斌, 朱晔荣. 异常血流动力对HUVEC胆固醇代谢的影响及其致AS的机制[J]. 徐州医科大学学报, 2022, 42(3): 163-169. DOI: 10.3969/j.issn.2096-3882.2022.03.002
    The effect of abnormal blood flow power on cholesterol me<x>tabolism of HUVEC and the mechanism of its-induced atherosclerosis.[J]. Journal of Xuzhou Medical University, 2022, 42(3): 163-169. DOI: 10.3969/j.issn.2096-3882.2022.03.002
    Citation: The effect of abnormal blood flow power on cholesterol me<x>tabolism of HUVEC and the mechanism of its-induced atherosclerosis.[J]. Journal of Xuzhou Medical University, 2022, 42(3): 163-169. DOI: 10.3969/j.issn.2096-3882.2022.03.002

    异常血流动力对HUVEC胆固醇代谢的影响及其致AS的机制

    The effect of abnormal blood flow power on cholesterol me<x>tabolism of HUVEC and the mechanism of its-induced atherosclerosis.

    • 摘要: 目的 通过研究异常血流动力对人脐静脉内皮细胞摄取、合成及外排胆固醇的影响。进一步探讨异常血流动力和胆固醇代谢在动脉粥样硬化形成机制中的作用。方法 待细胞生长良好后,换用新的含有LDL和ApoA-I的培养液,同时施加作用力。按照细胞所受作用力不同,随机分为应力组、壁面压力组、正常组和不加力组。在各自作用力的作用下培养24小时。收集细胞和培养液待用。用酶法检测四组培养液中LDL浓度和胆固醇浓度。用高效液相色谱法检测人脐静脉内皮细胞内和细胞膜中胆固醇的含量。分别用实时定量RT-PCR法和蛋白免疫印迹法检测LDLR、HMG-CR、ABCA1的mRNA和蛋白表达水平。结果 与不加力组相比较,应力组培养液中LDL含量明显减少,细胞内胆固醇含量明显增高。而且LDLR和HMG-CR的mRNA和蛋白表达明显增高。壁面压力组培养液中胆固醇含量明显增高,细胞膜中胆固醇含量明显降低,而且ABCA1的mRNA和蛋白表达明显增高。正常组培养液中LDL含量明显降低,胆固醇含量明显增高,而且LDLR、HMG-CR和ABCA1的mRNA和蛋白表达均明显增高。结论 应力通过上调LDLR和HMG-CR的mRNA和蛋白的表达促进VEC摄取LDL和合成胆固醇,壁面压力通过上调ABCA1的mRNA和蛋白的表达促进VEC膜外排胆固醇。异常血流动力使血管内皮细胞胆固醇代谢平衡紊乱进而引起AS。

       

      Abstract: Aim To study the effects of abnormal blood flow power on uptake, synthesis and efflux of cholesterol in human umbilical vein endothelial cells(HUVECs). To further explore the role of abnormal blood flow power and cholesterol me<x>tabolism in the formation of atherosclerosis. Methods When the cells grew well, a new culture solution containing LDL and ApoA-I was used, and a force was applied. The cells were randomly divided into stress group, wall pressure group, normal group and no stress group according to the force acting on the cells. They were cultured for 24 hours under the action of the respective forces. Collect cells and culture medium to be used. The LDL and cholesterol concentrations in the four groups of culture medium were detected by enzymatic method. The content of intracellular cholesterol and The cholesterol content of cell membrane were determined by HPLC. The mRNA and protein ex<x>pression levels of LDLR, HMG-CR and ABCA1 were detected by real-time quantitative RT-PCR and western blot respectively. Results compared with the no stress group, the content of LDL in the culture medium of the stress group was significantly decreased and the content of intracellular cholesterol was significantly increased. Moreover, the ex<x>pression of mRNA and protein of LDLR and HMG-CR was significantly increased. In the wall pressure group, the cholesterol content in the culture medium was significantly increased, the cholesterol content in the cell membrane was significantly decreased, and the ex<x>pression of ABCA1mRNA and protein was significantly increased. In the normal group, LDL was significantly decreased and cholesterol significantly increased in the culture medium, and the ex<x>pression of mRNA and protein of LDLR、HMG-CR and ABCA1 was significantly increased. Conclusions stress promotes the uptake of LDL and synthesis cholesterol by up-regulating the ex<x>pression of LDLR and HMG-CR mRNA and protein, and wall pressure promotes cholesterol efflux by up-regulating the ex<x>pression of ABCA1mRNA and protein. Abnormal blood flow power disturbs the cholesterol me<x>tabolism balance of vascular endothelial cells and causes AS.

       

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