王如科 孙源源 韩建一 逍遥 史怀璋.银杏叶提取物对过氧化氢刺激下的血管内皮细胞的影响[J].现代生物医学进展英文版,2014,14(26):5038-5041. |
银杏叶提取物对过氧化氢刺激下的血管内皮细胞的影响 |
Effects of Ginkgo Biloba Extract on Hydrogen Peroxide-stimulatedVascular Endothelial Cells |
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DOI: |
中文关键词: 血管内皮细胞 自由基清除剂 内质网应激 细胞凋亡 银杏叶提取物 |
英文关键词: Vascular endothelial cells Radical scavenger Endoplasmic reticulumstress Apoptosis Ginkgo biloba extract |
基金项目:吴阶平医学基金项目(320.6750.12189) |
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中文摘要: |
目的:探讨银杏叶提取物对血管内皮细胞的保护作用及可能的保护机制。方法:进行血管内皮细胞培养。用过氧化氢(H2O2)
处理血管内皮细胞建立细胞凋亡模型。将细胞分为四组:空白对照组、H2O2处理组、单独银杏叶提取物处理组、银杏叶提取物预处
理组(提前2h 给药后H2O2处理)。进行MTT 检测细胞的相对活力、RT-PCR 检测目的基因CHOP 的表达、Western Blot分析目的
蛋白CHOP 的表达等。结果:与对照处理组比较,H2O2处理组细胞凋亡率、CHOPmRNA相对表达及CHOP蛋白表达量明显升高。
与H2O2处理组比较,银杏叶提取物预处理组细胞凋亡指数、CHOPmRNA 相对表达及CHOP 蛋白表达量明显降低(P<0.05)。结
论:作为一种清除自由基、抗氧化、抗衰老药物,银杏叶提取物可能通过调节CHOP 蛋白选择性地抑制过度的内质网应激来保护
血管内皮细胞。 |
英文摘要: |
Objective:To investigate the protective effects of the Ginkgo biloba extract on vascular endothelial cells and its
possible mechanisms.Methods:The endothelial cells of blood vessels were cultured. The endothelial cells apoptosis model was
established by treatment with hydrogen peroxide (H2O2). Then divide the cells into four groups: blank control group, H2O2-treated group,
single ginkgo biloba extract-treated group, ginkgo biloba extract pretreatment group (giving H2O2 at 2 h after administration of ginkgo
biloba extract). The relative vitality were determined by MTT test cells. The expressions of gene CHOP were detected by RT - PCR, and
the CHOP target protein expressions were detected by western blot analysis.Results:Compared with the control, the cells apoptosis rate,
CHOPmRNA relative expression and CHOP protein expression was significantly increased in the H2O2-treated group. Compared with
H2O2-treated group, the cells apoptosis rate, CHOPmRNA relative expression and CHOP protein expression was significantly reduced in
the ginkgo biloba extract pretreatment group (P<0.05).Conclusion:As an antioxidant, free-radical scavenging and anti-aging medicine,
Ginkgo biloba extract may protect endothelial cells by regulating CHOP protein and selectively inhibiting excessive endoplasmic
reticulumstress. |
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