PI3K/AKT/mTOR通路
伊诺斯
内分泌学
内科学
蛋白激酶B
促卵泡激素
脐静脉
化学
生物
细胞凋亡
医学
促黄体激素
激素
一氧化氮
一氧化氮合酶
生物化学
体外
作者
Jingyu Piao,Yifan Yin,Ya-Ru Zhao,Yi Han,Huixia Zhan,Duosheng Luo,Junpeng Guo
出处
期刊:Journal of Vascular Research
[S. Karger AG]
日期:2022-01-01
卷期号:59 (6): 358-368
被引量:3
摘要
<b><i>Objective:</i></b> Follicle-stimulating hormone (FSH) level changes may be another reason for increasing the risk of cardiovascular disease. In this study, we aimed to investigate the role of FSH in atherosclerosis and its underlying mechanism. <b><i>Methods:</i></b> ApoE<sup>−/−</sup> mice were divided into 4 groups, namely, the sham group, bilaterally orchidectomized group, FSH group, and testosterone-only group. Blood lipid and hormone levels were tested, aorta Oil Red O staining; the levels of NF-κB, Akt, eNOS, and FSH receptors in the aorta were measured by Western blotting. Expression of VCAM-1 was detected via Western blotting and immunohistochemical staining. Human umbilical vein endothelial cells (HUVECs) were used to induce endothelial injury model by adding FSH, and the levels of NF-κB, Akt, eNOS, and FSHR were tested in HUVECs. <b><i>Results:</i></b> FSH treatment exacerbated atherosclerotic lesions in ApoE<sup>−/−</sup> mice. Moreover, FSH could promote the expression of VCAM-1 protein in HUVECs, and this effect was possibly mediated by the activation of NF-κB, while NF-κB activation was further enhanced by the activation of the PI3K/Akt/eNOS pathway. FSH failed to activate Akt and NF-κB in the presence of the PI3K inhibitor LY294002 in HUVECs. <b><i>Conclusion:</i></b> FSH promoted the development of atherosclerosis by increasing VCAM-1 protein expression via activating PI3K/Akt/NF-κB pathway.
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