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. 2019 Jun 11;9:8481. doi: 10.1038/s41598-019-44834-8

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© The Author(s) 2019

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Ang II increases ER Stress and inflammation, while RAS inhibitors reduce inflammation in 3T3-L1 adipocytes in vitro: Adipocytes were treated with different concentration of Ang II (A). Differentiated adipocytes treated with media (control), Angiotensin II (Ang II), A + T (Ang II & Telmisartan), A + P-186 (Ang II & P-186), & A + T + P-186 (Ang II, Telmisartan & P-186) and ER stress as well as inflammatory markers were measured. Ang II (10 nM) treatment significantly (p < 0.05) increased ER stress markers (Chop, Atf4, Bip) (B–D) and pro inflammatory markers such as Il-6 and nuclear factor kappa B (Nfkb) (E,F). Ang II antagonist Telmisartan significantly (p < 0.05) reduced the Ang II induced ER stress and inflammation (B–F). Common letters indicate no significance. Data is presented as mean ± SEM (n = 5). p < 0.05.