Alginate oligosaccharide protects endothelial cells against oxidative stress injury via integrin-α/FAK/PI3K signaling

被引:31
作者
Zhao, Jing [1 ]
Han, Yue [2 ]
Wang, Zongqiu [1 ]
Zhang, Rui [3 ]
Wang, Guimei [1 ]
Mao, Yongjun [1 ]
机构
[1] Qingdao Univ, Affiliated Hosp, Dept Geriatr, Qingdao 266003, Peoples R China
[2] Qingdao Univ, Affiliated Hosp, Dept Gastroenterol, Qingdao 266003, Peoples R China
[3] Qingdao Univ, Affiliated Hosp, Dept Cardiol, Qingdao 266003, Peoples R China
基金
中国国家自然科学基金;
关键词
AOS; Apoptosis; H2O2; HUVEC; Atherosclerosis; ENDOPLASMIC-RETICULUM;
D O I
10.1007/s10529-020-03010-z
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Alginate oligosaccharide (AOS) was reported to possess antioxidant and free radical scavenging activities, but the specific effects and mechanisms remain unclear. We investigated the effects of AOS on H2O2-induced oxidative stress and apoptosis in human umbilical vein endothelial cells (HUVECs) and the associated mechanisms. HUVECs were treated with 100-800 mu M hydrogen peroxide (H2O2) for various periods (12, 24, and 36 h) to establish an in vitro oxidative stress and apoptosis HUVEC model. AOS protects HUVEC cells against oxidative stress-induced apoptosis by decreasing the expression levels of caspase 3 and Bax, and increasing Bcl-2 expression. Microarray assay, real-time PCR and western blot results revealed that AOS was able to effectively suppress H2O2-induced apoptosis via regulated integrin-alpha/FAK/PI3K pathway by influencing the expression of integrin-alpha, FAK, PI3K, PTEN, P21, and CDK2. In conclusion, our study suggests that AOS can protect endothelial cells against oxidative stress injury caused by H2O2, providing novel alternative strategies to prevent atherosclerosis in the future.
引用
收藏
页码:2749 / 2758
页数:10
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