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. 2020 Jun 5;20:269. doi: 10.1186/s12872-020-01492-3

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — Overexpression of PGC-1α rescued the inhibitory effect of β1AA on VEGF expression. a Raw data of results of WB test. β1AA increased the protein expression of β1AR and caspase3, and inhibited the protein expression of VEGF. But the overexpression of PGC-1α inhibited the effect of β1AA. b Overexpression of PGC-1α increased the VEGF mRNA expression and rescued the inhibitory effect of β1AA. c ELISA test for secreted VEGF in the supernatant of the medium. Overexpression of PGC-1α also rescued the inhibitory effect of β1AA on the VEGF secretion. d and e overexpression of PGC-1α increased the NRF1 and ERRα mRNA expression and rescued the inhibitory effect of β1AA. **, P ≤ 0.01. Group data presented by mean ± SEM