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大米α-球蛋白肽YGEGSSEEG对TNF-α诱导的血管内皮细胞损伤的影响

鞠志远 王丽丽 刘丽娅 周闲容 周素梅 佟立涛

中国药理学通报2018,Vol.34Issue(4):501-507,7.
中国药理学通报2018,Vol.34Issue(4):501-507,7.DOI:10.3969/j.issn.1001-1978.2018.04.013

大米α-球蛋白肽YGEGSSEEG对TNF-α诱导的血管内皮细胞损伤的影响

Effects of rice peptide YGEGSSEEG on improving endothelial cell injury induced by tumor necrosis factor

鞠志远 1王丽丽 1刘丽娅 1周闲容 1周素梅 1佟立涛1

作者信息

  • 1. 中国农业科学院农产品加工研究所,农业部农产品加工综合性重点实验室,北京 100193
  • 折叠

摘要

Abstract

Aim To investigate the peptides and its protection for vascular endothelial cells, derived from the absorbed components of rice α-globulin,which was shown to be effective in anti-atherosclerosis. Methods The amino acid sequence was purified by gel chro-matography and RP-HPLC, and determined by ESI/MS. Then the peptide was chemically synthesized. Hu-man umbilical vein endothelial cell injury model was induced by tumor necrosis factor-α. The cell viability was measured by cell counting kit to screen the appro-priate peptide intervention concentration. The apoptotic rate was detected by flow cytometry. Bcl-2, Bax, p-p38, vascular cell adhesion molecule and the protein expression level of NF-κB signaling pathway were de-tected by Western blot and immunofluorescent stai-ning. Results Apoptosis of HUVECs induced by TNF-α was significantly increased by YGEGSSEEG, which also regulated expression of Bcl-2/Bax proteins and inhibited phosphorylation of p38 protein. Besides, the peptide suppressed the production of VCAM-1, ICAM-1 and activation of NF-κB pathway. While it did not significantly improve the oxidative stress response in HUVECs. Conclusion Peptide YGEGSSEEG pro-tects vascular endothelial cells through suppressing ap-optosis and expression of adhesion molecules.

关键词

大米α-球蛋白肽/人脐静脉内皮细胞/细胞凋亡/黏附分子/NF-κB信号通路/Bcl-2/Bax蛋白

Key words

rice α-globulin peptide/HUVECs/apop-tosis/adhesion molecules/NF-κB signaling pathway/Bcl-2/Bax

分类

医药卫生

引用本文复制引用

鞠志远,王丽丽,刘丽娅,周闲容,周素梅,佟立涛..大米α-球蛋白肽YGEGSSEEG对TNF-α诱导的血管内皮细胞损伤的影响[J].中国药理学通报,2018,34(4):501-507,7.

基金项目

国家自然科学基金资助项目(No 31401505) (No 31401505)

中国药理学通报

OA北大核心CSCDCSTPCD

1001-1978

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