| 陈文豪 陈浩 赵达君 乔慧莲 易定华.番茄红素对血管内皮细胞氧化应激损伤的作用及机制研究[J].,2014,14(11):2037-2042 |
| 番茄红素对血管内皮细胞氧化应激损伤的作用及机制研究 |
| The Protective Effects and Mechanismof Lycopene Against H2O2 inducedInjury in Vascular Endothelial Cells |
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| DOI： |
| 中文关键词: 番茄红素 人脐静脉内皮细胞 氧化应激 凋亡 p38MAPK信号通路 |
| 英文关键词: Lycopene Human umbilical vein endothelial cells Oxidative stress Apoptosis P38MAPK signal pathway |
| 基金项目:国家自然科学基金项目（81070183；81100137） |
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| 中文摘要: |
| ：观察番茄红素（lycopene，LYC）对于血管内皮细胞功能的作用，探讨其作用机制。方法：人脐静脉内皮细胞（HUVECs）
处理实验分组：对照组，H2O2组，H2O2+ LYC 组（1、2、4、8 umolL-1）。MTT 法检测HUVECs 存活率；免疫印迹法（Western blot）检测
p38MAPK 蛋白磷酸化水平、抗凋亡蛋白B 淋巴细胞/白血病-2（bcl-2）及线粒体凋亡通路相关蛋白bax 的表达；细胞黏附能力测
定和伤口愈合实验检测HUVECs 粘附率和迁移率；TUNEL 法检测HUVECs 凋亡率；ELASA法测定HUVECs 内活性氧（ROS），
超氧化物歧化酶（SOD），乳酸盐脱氢酶（LDH）释放量和caspase-3 的活性。结果：H2O2损伤后HUVECs 存活率显著降低（P<0.01），
凋亡率显著增加（P<0.01），黏附和迁移能力显著降低（P<0.01），bax 和p-p38MAPK 的表达上调，bcl-2 的表达下调，并且ROS、
LDH 的释放和caspase-3 的活性增加（P<0.01），SOD的释放减少。而LYC的预处理可以明显逆转H2O2以上作用。结论：H2O2氧化
应激损伤中，LYC 保护内皮细胞可能与其抗过氧化损伤细胞凋亡，抑制异常的p38MAPK 信号通路有关。 |
| 英文摘要: |
| Objective:To observe the effect of lycopene (LYC) in human umbilical endothelial cells (HUVECs) and investigate
the mechanismof LYC. Methods:The groups of cells were divided as below: control group, H2O2 treatment group, H2O2 treatment +LYC
(1、2、4、8 umolL-1) treatment group. The survival rate of HUVECs was detected by MTT method; The indicator were detected by
Western blot, which included the phosphorylation level of p38MAPK and the expression of mitochondrial apoptosis pathway proteins
(bax), B-lymphocyte / leukemia -2 (bcl-2) protein; The adhesive rate and migration of HUVECs was detected by the cellular adhesion
ability assay and the wound healing assay; The apoptosis rate of HUVECs was detected by TUNEL; The indicator were detected by
ELISA, which included the production of Reactive oxygen species (ROS), superoxide dismutase (SOD), lactate dehydrogenase (LDH)
and caspase-3 activity. Results:After being treated with H2O2, the HUVECs survival rate was distinctly decreased (P<0.01), the HUVECs
apoptosis rate was distinctly increased (P<0.01), the HUVECs adhesion and migration ability was distinctly reduced (P<0.01), The
phosphorylation level of p38MAPK and the expression of bax protein was distinctly down-regulated (P<0.01), and the expression of
bcl-2 protein was distinctly up-regulated (P<0.01), the production of ROS, LDH and caspase-3 activity was distinctly increased (P<0.01),
the production of SOD was distinctly decreased (P<0.01). Moreover, after the treatment with LYC, these effects has been reversed. Conclusion:LYC can anti-oxidation stress injury induced by H2O2 of HUVECs via its capacity of anti-apoptosis and inhibition of
abnormal p38MAPK signal pathway. |
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