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机构地区:[1]温州医学院第二附属医院神经内科,浙江温州325027
出 处:《中国病理生理杂志》2007年第4期699-701,共3页Chinese Journal of Pathophysiology
基 金:温州市科技计划基金资助项目(No.Y2003A008)
摘 要:目的:明确同型半胱氨酸(Hcy)对内皮细胞凋亡的影响以及叶酸的拮抗作用,阐明Bax和Bcl-2在同型半胱氨酸诱导内皮细胞凋亡及叶酸拮抗中的作用。方法:用不同浓度的Hcy处理内皮细胞后,应用末端转移标记技术(TUNEL)以及Annexin V/PI染色加流式细胞术了解细胞凋亡状态,免疫组化方法检测Bax、Bcl-2的表达。结果:Hcy能促进细胞凋亡,叶酸具有拮抗作用。Hcy能促进细胞Bax、Bcl-2的表达,上调Bax/Bcl-2比值,叶酸能减少细胞表达Bax及Bcl-2,下调Bax/Bcl-2比值。结论:Bax、Bcl-2参与了Hcy诱导内皮细胞凋亡以及叶酸拮抗作用的过程。AIM: To investigate the effects of homocysteine (Hcy) on apoptosis in SV40 -transformed aortic rat endothelial cell line and the anti - apoptosis effects of folic acid. METHODS: Cells were treated with different concentrations of Hcy and folic acid, apoptosis was detected by TUNEL and annexin - V/PI staining methods. Immunohistochemical assay was used to examine the expression of Bax and Bcl - 2 in all groups. RESULTS : Both armexin - V/PI staining and TUNEL method showed that Hcy increased endothelial apoptosis in a dose - dependent manner, while folic acid reduced cell apeptosis. Hcy increased expression of Bax and Bcl -2 in endothelial cells, and folic acid decreased it. Bax/Bcl -2 ratio in 0. 5 mmol/L Hcy and 5.0 mmol/L Hcy group were upregulated compared with control group ( P 〈 0. 05 and P 〈 0. 01, respectively). Addition of 0. 1 mmol/L folic acid decreased Bax/Bcl -2 ratio compared with the corresponding group without folic acid (P 〈0. 05). Correlation analysis showed a strong relation between Bax/Bcl -2 ratio and apeptotic rate (P 〈 0. 01 ). CONCLUSION: Folic acid attenuates the apeptosis induced by Hcy in endothelial cells. Hcy may promote endothelial cell apeptosis via upregulation of Bax/Bc1-2 ratio, which can be partially antagonized by folic acid.
关 键 词:高半胱氨酸 叶酸 内皮细胞 细胞凋亡 蛋白质BAX 蛋白质BCL-2
分 类 号:R541[医药卫生—心血管疾病]
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