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. 2022 Jan 20;19:6. doi: 10.1186/s12986-021-00639-z

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© The Author(s) 2022

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. 3 — The important suggested mechanisms for the effect of Propolis on dyslipidemia in A liver by inhibiting cholesterol and triglyceride synthesis and inducing ß-oxidation and cholesterol-bile acid turnover, B gastrointestinal system by inhibiting the absorption of triglyceride and probably cholesterol, and C adipose tissue by regulation of fat accumulation and lipolysis and dyslipidemia-induced renal damage. Abbreviations: CYP7A1, Cholesterol 7α-hydroxylase; SREBP, Sterol regulatory element-binding proteins; FAS, fatty acid synthase; ACAC-α, acetyl-CoA carboxylase α; HMGCS-1, 3-hydroxy-3-methylglutaryl-Coenzyme A synthase 1; HMGCR, 3-hydroxy-3-methylglutaryl-Coenzyme A reductase; SQLE, Squalene Epoxidase; PPAR, peroxisome proliferator-activated receptor; FA, fatty acid; TG, triglyceride; ROS, reactive oxygen species; NF-κB, nuclear factor kappa B; ECM, extracellular matrix