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. 2021 Feb 9;11:620159. doi: 10.3389/fphar.2020.620159

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Copyright © 2021 Liu, Yin, Li, Jiang, Zhang, Zhang and Li.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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ST attenuated AngⅡ-induced HUVECs dysfunction. (A) Representative images and quantitative analysis of migration assay (HE stain, 100×). (B) Representative images and quantitative analysis of adhesion assay (HE stain, 100×). (C) Representative images and quantitative analysis of tube formation assay in vitro (200×). The number of tubular structures in the field represented the angiogenesis capacity of vascular endothelia. (D) Western blot analysis of eNOS and p-eNOS expression in control, AngⅡ and AngⅡ+ST groups. The data were presented in fold of control. (E) ELISA analysis of the level of NO in above three groups. (F) ELISA analysis of the level of ET-1 in above three groups. All data except ELISA analysis were shown as mean ± SD (error bars) from three independent biological repeats experiments, each of which included three technical repeats. ^* p < 0.05; ^** p < 0.01.