Gegen Qinlian Decoction Modulates Atherosclerosis and Lipid Metabolism Through Cellular Interplay and Signaling Pathways
- Authors: Zhang Z.1, Zhou Y.2, Lv Q.1, Gao K.3, Li Z.1, Miao Q.3, Shen L.3
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Affiliations:
- Department of Digestive Endocrinology, Beijing Fengtai Hospital of Integrated traditional and Western Medicine
- Department of Nephrology Endocrinology, Beijing Hospital of Integrated traditional and Western Medicine
- Institute of Basic Theory for Chinese Medicine, China Academy of Chinese Medical Sciences
- Issue: Vol 27, No 17 (2024)
- Pages: 2609-2621
- Section: Chemistry
- URL: https://vietnamjournal.ru/1386-2073/article/view/645275
- DOI: https://doi.org/10.2174/0113862073285562240305113728
- ID: 645275
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Full Text
Abstract
Objective:The objective of this study is to investigate Gegen Qinlian decoction (GQD) effects on lipid metabolism and explore its mechanism for preventing and treating atherosclerosis.
Methods:An atherosclerotic rat model was established;, and after an 8-week high-fat diet, atherosclerosis and non-alcoholic fatty liver disease were assessed. Subsequently, GQD was administered at low and high doses. Histopathological aortic wall changes, hepatic lipid deposition, and blood lipid changes were evaluated. ELISA indicated the influence of TNF-α and IL-13, and Western blotting revealed MerTK, ABCA1, and LXR-α expression. A foam macrophage model was established, and Cell activity was detected by the MTT method. ELISA indicated the influence of PPAR-γ. The expression of ABCA1, ABCA7, ABCG1, GAS6, MerTK, SCARB1, LXR- α and LXR-β mRNA were detected by qPCR, and Western blotting revealed MerTK and LXR-α expression. The impact of drug-containing serum of GQD on efferocytosis-related factors was studied.
Results:GQD improved atherosclerosis and non-alcoholic fatty liver disease and reduced serum low-density lipoprotein levels in the high-dose group. The high- and low-dose groups showed upregulated ABCA1, MerTK, and LXR-α expression in blood vessels and the liver, respectively. GQD decreased serum TNF-α and increased IL-13 levels. PPAR-γ expression was elevated in the high-, and low-dose groups. In the high-and low-dose groups, ABCA7, GAS6, SCARB1, and LXR-α, ABCA1 and MerTK, and ABCG1 gene expression were upregulated, respectively. Both low- and high-dose serum-containing drugs promoted LXR-β gene expression, and LXR-α protein expression was improved in the high-dose group.
Conclusion:GQD improves rat atherosclerosis and hepatic lipid metabolism by regulating PPAR-γ, LXR-α, LXR-β, ABCA1, ABCA7, and ABCG1 expression and augmenting cellular intercalation through the GAS6/TAM pathway
About the authors
Zhiwei Zhang
Department of Digestive Endocrinology, Beijing Fengtai Hospital of Integrated traditional and Western Medicine
Email: info@benthamscience.net
Yu Zhou
Department of Nephrology Endocrinology, Beijing Hospital of Integrated traditional and Western Medicine
Email: info@benthamscience.net
Qin Lv
Department of Digestive Endocrinology, Beijing Fengtai Hospital of Integrated traditional and Western Medicine
Email: info@benthamscience.net
Kun Gao
Institute of Basic Theory for Chinese Medicine, China Academy of Chinese Medical Sciences
Email: info@benthamscience.net
Zhiguo Li
Department of Digestive Endocrinology, Beijing Fengtai Hospital of Integrated traditional and Western Medicine
Email: info@benthamscience.net
Qing Miao
Institute of Basic Theory for Chinese Medicine, China Academy of Chinese Medical Sciences
Email: info@benthamscience.net
Li Shen
Institute of Basic Theory for Chinese Medicine, China Academy of Chinese Medical Sciences
Author for correspondence.
Email: info@benthamscience.net
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