文献类型：期刊文献

英文题名：In Vitro Vascular-Protective Effects of a Tilapia By-Product Oligopeptide on Angiotensin II-Induced Hypertensive Endothelial Injury in HUVEC by Nrf2/NF-κB Pathways

作者：Chen, Jiali[1];Gong, Fang[1];Chen, Mei-Fang[1];Li, Chengyong[2,3];Hong, Pengzhi[1];Sun, Shengli[2];Zhou, Chunxia[1];Qian, Zhong-Ji[2,3]

机构：[1]Guangdong Ocean Univ, Coll Food Sci & Technol, Zhanjiang 524088, Peoples R China;[2]Guangdong Ocean Univ, Sch Chem & Environm Sci, Zhanjiang 524088, Peoples R China;[3]Guangdong Ocean Univ, Shenzhen Inst, Shenzhen 518108, Peoples R China

年份：2019

卷号：17

期号：7

外文期刊名：MARINE DRUGS

收录：SCI-EXPANDED(收录号：WOS:000478650600027)、、Scopus(收录号：2-s2.0-85069695579)、WOS

基金：The study was supported by the Yangfan Scarce Top Talent Project of Guangdong Province (201433009), Program for Scientific Research Start-Up Funds of Guangdong Ocean University [to Zhong-Ji Qian], Innovation and Strong University Project (2013050204) and the Development Project about Marine Economy Demonstration of Zhanjiang City (2017C8B1).

语种：英文

外文关键词：tilapia; HUVEC; angiotensin II; NF-kappa B; Nrf2; endothelial dysfunction

外文摘要：Angiotensin II (Ang II) is closely involved in endothelial injury during the development of hypertension. In this study, the protective effects of the tilapia by-product oligopeptide Leu-Ser-Gly-Tyr-Gly-Pro (LSGYGP) on oxidative stress and endothelial injury in Angiotensin II (Ang II)-stimulated human umbilical vein endothelial cells (HUVEC) were evaluated. LSGYGP dose-dependently suppressed the fluorescence intensities of nitric oxide (NO) and reactive oxygen species (ROS), inhibited the nuclear factor-kappa B (NF-kappa B) pathway, and reduced inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and endothelin-1 (ET-1) expression, as shown by western blot. In addition, it attenuated the expression of gamma-glutamyltransferase (GGT) and heme oxygenase 1 (HO-1), as well as increasing superoxide dismutase (SOD) and glutathione (GSH) expression through the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Other experiments revealed that LSGYGP increased the apoptotic inhibition ratio between cleaved-caspase-3/procaspase-3, reduced expressions of pro-apoptotic ratio between Bcl-2/Bax, inhibited phosphorylation of mitogen-activated protein kinases (MAPK), and increased phosphorylation of the serine/threonine kinase (Akt) pathway. Furthermore, LSGYGP significantly decreased Ang II-induced DNA damage in a comet assay, and molecular docking results showed that the steady interaction between LSGYGP with NF-kappa B may be attributed to hydrogen bonds. These results suggest that this oligopeptide is effective in protecting against Ang II-induced HUVEC injury through the reduction of oxidative stress and alleviating endothelial damage. Thus, it has the potential for the therapeutic treatment of hypertension-associated diseases.