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<article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="research-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Combinatorial Chemistry &amp; High Throughput Screening</journal-id><journal-title-group><journal-title xml:lang="en">Combinatorial Chemistry &amp; High Throughput Screening</journal-title><trans-title-group xml:lang="ru"><trans-title>Combinatorial Chemistry &amp; High Throughput Screening</trans-title></trans-title-group></journal-title-group><issn publication-format="print">1386-2073</issn><issn publication-format="electronic">1875-5402</issn><publisher><publisher-name xml:lang="en">Bentham Science</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">645275</article-id><article-id pub-id-type="doi">10.2174/0113862073285562240305113728</article-id><article-categories><subj-group subj-group-type="toc-heading"><subject>Chemistry</subject></subj-group><subj-group subj-group-type="article-type"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">Gegen Qinlian Decoction Modulates Atherosclerosis and Lipid Metabolism Through Cellular Interplay and Signaling Pathways</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Zhang</surname><given-names>Zhiwei</given-names></name><email>info@benthamscience.net</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name><surname>Zhou</surname><given-names>Yu</given-names></name><email>info@benthamscience.net</email><xref ref-type="aff" rid="aff2"/></contrib><contrib contrib-type="author"><name><surname>Lv</surname><given-names>Qin</given-names></name><email>info@benthamscience.net</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name><surname>Gao</surname><given-names>Kun</given-names></name><email>info@benthamscience.net</email><xref ref-type="aff" rid="aff3"/></contrib><contrib contrib-type="author"><name><surname>Li</surname><given-names>Zhiguo</given-names></name><email>info@benthamscience.net</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name><surname>Miao</surname><given-names>Qing</given-names></name><email>info@benthamscience.net</email><xref ref-type="aff" rid="aff3"/></contrib><contrib contrib-type="author"><name><surname>Shen</surname><given-names>Li</given-names></name><email>info@benthamscience.net</email><xref ref-type="aff" rid="aff3"/></contrib></contrib-group><aff id="aff1"><institution>Department of Digestive Endocrinology, Beijing Fengtai Hospital of Integrated traditional and Western Medicine</institution></aff><aff id="aff2"><institution>Department of Nephrology Endocrinology, Beijing Hospital of Integrated traditional and Western Medicine</institution></aff><aff id="aff3"><institution>Institute of Basic Theory for Chinese Medicine, China Academy of Chinese Medical Sciences</institution></aff><pub-date date-type="pub" iso-8601-date="2024-09-01" publication-format="electronic"><day>01</day><month>09</month><year>2024</year></pub-date><volume>27</volume><issue>17</issue><issue-title xml:lang="ru"/><fpage>2609</fpage><lpage>2621</lpage><history><date date-type="received" iso-8601-date="2025-01-07"><day>07</day><month>01</month><year>2025</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2024, Bentham Science Publishers</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="en">Bentham Science Publishers</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/></permissions><self-uri xlink:href="https://rjpbr.com/1386-2073/article/view/645275">https://rjpbr.com/1386-2073/article/view/645275</self-uri><abstract xml:lang="en"><p id="idm46041443729440">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.</p><p id="idm46041443733440">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.</p><p id="idm46041443737408">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.</p><p id="idm46041443742464">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</p></abstract><kwd-group xml:lang="en"><kwd>Gegen qinlian decoction</kwd><kwd>macrophage cytoburial</kwd><kwd>atherosclerosis</kwd><kwd>lipid metabolism</kwd><kwd>PPAR&amp;amp</kwd><kwd>gamma</kwd><kwd>/LXRα/ABCA1</kwd><kwd>GAS6/TAM.</kwd></kwd-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Martinet, W.; Coornaert, I.; Puylaert, P.; De Meyer, G.R.Y. Macrophage death as a pharmacological target in atherosclerosis. Front. 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