Biochanin A Regulates Cholesterol Metabolism Further Delays the Progression of Nonalcoholic Fatty Liver Disease

Yan Fan,1,* Long-Teng Yan,2,* Zheng Yao,2 Guang-Yi Xiong2 1Department of Anatomy, Histology, and Embryology, School of Basic Medical Science, Kunming Medical University, Kunming, Yunnan, 650500, People’s Republic of China; 2Key Laboratory of Microcosmic Syndrome Differentiation, Scho...

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Autores principales: Fan Y, Yan LT, Yao Z, Xiong GY
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Publicado: Dove Medical Press 2021
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spelling oai:doaj.org-article:a9279746a3b04a009d334bc7b721ceba2021-12-02T18:34:24ZBiochanin A Regulates Cholesterol Metabolism Further Delays the Progression of Nonalcoholic Fatty Liver Disease1178-7007https://doaj.org/article/a9279746a3b04a009d334bc7b721ceba2021-07-01T00:00:00Zhttps://www.dovepress.com/biochanin-a-regulates-cholesterol-metabolism-further-delays-the-progre-peer-reviewed-fulltext-article-DMSOhttps://doaj.org/toc/1178-7007Yan Fan,1,&ast; Long-Teng Yan,2,&ast; Zheng Yao,2 Guang-Yi Xiong2 1Department of Anatomy, Histology, and Embryology, School of Basic Medical Science, Kunming Medical University, Kunming, Yunnan, 650500, People’s Republic of China; 2Key Laboratory of Microcosmic Syndrome Differentiation, School of Basic Medicine, Yunnan University of Chinese Medicine, Kunming, Yunnan, 650500, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Zheng Yao; Guang-Yi XiongKey Laboratory of Microcosmic Syndrome Differentiation, School of Basic Medicine, Yunnan University of Chinese Medicine, No. 1076, Yuhua Road, Chenggong District, Kunming, Yunnan, 650500, People’s Republic of ChinaTel/Fax +86 189 0871 9365Email zhengyaomail@126.com; 307924002@qq.comPurpose: To discover the possible target of biochanin A (BCA) in the lipid metabolism pathway and further explore its mechanism to nonalcoholic fatty liver disease (NAFLD).Methods: We adopted a high-fat and high-glucose diet for 12 weeks to build the NAFLD rat model, which was then treated with different proportions of BCA for 4 weeks. General condition, body weight, Lee index, and liver index were then evaluated. Furthermore, blood lipid level and insulin resistance (IR) were detected. Moreover, hematoxylin and eosin and oil red O staining were used to observe the pathological changes in the liver. Finally, Western blotting was used to detect the protein expression levels of CYP7A1, HMGCR, LDLR, PPAR-α, PPAR-γ, and SREBP-1c in the liver.Results: The vital signs of rats in each group were stable. The treatment with BCA effectively reduced Lee index and liver index (F = 104.781, P < 0.05); however, the weight was not effected in each group. Additionally, BCA effectively reduced the related lipid metabolism indexes of NAFLD, such as total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL), blood glucose, insulin, IR (F =12.463 (TC), 6.909 [TG], and 15.3 effected 75 [LDL], P < 0.05), and increased HDL (F = 11.580, P < 0.05). We observed that BCA could significantly improve steatosis and inflammatory cell infiltration in liver slices. Furthermore, BCA significantly increased the CYP7A1, LDLR, and PPAR-α protein expression in the liver and downregulated the HMGCR, SREBP-1c, and PPAR-γ protein expression.Conclusion: BCA could delay the liver damage of NAFLD induced by a high-fat diet, regulate the blood lipid level, and improve the expression of lipid metabolism-related genes in rats.Keywords: biochanin A, nonalcoholic fatty liver disease, NAFLD, cholesterol metabolismFan YYan LTYao ZXiong GYDove Medical Pressarticlebiochanin a;nonalcoholic fatty liver diseasenafldcholesterol metabolismSpecialties of internal medicineRC581-951ENDiabetes, Metabolic Syndrome and Obesity: Targets and Therapy, Vol Volume 14, Pp 3161-3172 (2021)
institution DOAJ
collection DOAJ
language EN
topic biochanin a;nonalcoholic fatty liver disease
nafld
cholesterol metabolism
Specialties of internal medicine
RC581-951
spellingShingle biochanin a;nonalcoholic fatty liver disease
nafld
cholesterol metabolism
Specialties of internal medicine
RC581-951
Fan Y
Yan LT
Yao Z
Xiong GY
Biochanin A Regulates Cholesterol Metabolism Further Delays the Progression of Nonalcoholic Fatty Liver Disease
description Yan Fan,1,&ast; Long-Teng Yan,2,&ast; Zheng Yao,2 Guang-Yi Xiong2 1Department of Anatomy, Histology, and Embryology, School of Basic Medical Science, Kunming Medical University, Kunming, Yunnan, 650500, People’s Republic of China; 2Key Laboratory of Microcosmic Syndrome Differentiation, School of Basic Medicine, Yunnan University of Chinese Medicine, Kunming, Yunnan, 650500, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Zheng Yao; Guang-Yi XiongKey Laboratory of Microcosmic Syndrome Differentiation, School of Basic Medicine, Yunnan University of Chinese Medicine, No. 1076, Yuhua Road, Chenggong District, Kunming, Yunnan, 650500, People’s Republic of ChinaTel/Fax +86 189 0871 9365Email zhengyaomail@126.com; 307924002@qq.comPurpose: To discover the possible target of biochanin A (BCA) in the lipid metabolism pathway and further explore its mechanism to nonalcoholic fatty liver disease (NAFLD).Methods: We adopted a high-fat and high-glucose diet for 12 weeks to build the NAFLD rat model, which was then treated with different proportions of BCA for 4 weeks. General condition, body weight, Lee index, and liver index were then evaluated. Furthermore, blood lipid level and insulin resistance (IR) were detected. Moreover, hematoxylin and eosin and oil red O staining were used to observe the pathological changes in the liver. Finally, Western blotting was used to detect the protein expression levels of CYP7A1, HMGCR, LDLR, PPAR-α, PPAR-γ, and SREBP-1c in the liver.Results: The vital signs of rats in each group were stable. The treatment with BCA effectively reduced Lee index and liver index (F = 104.781, P < 0.05); however, the weight was not effected in each group. Additionally, BCA effectively reduced the related lipid metabolism indexes of NAFLD, such as total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL), blood glucose, insulin, IR (F =12.463 (TC), 6.909 [TG], and 15.3 effected 75 [LDL], P < 0.05), and increased HDL (F = 11.580, P < 0.05). We observed that BCA could significantly improve steatosis and inflammatory cell infiltration in liver slices. Furthermore, BCA significantly increased the CYP7A1, LDLR, and PPAR-α protein expression in the liver and downregulated the HMGCR, SREBP-1c, and PPAR-γ protein expression.Conclusion: BCA could delay the liver damage of NAFLD induced by a high-fat diet, regulate the blood lipid level, and improve the expression of lipid metabolism-related genes in rats.Keywords: biochanin A, nonalcoholic fatty liver disease, NAFLD, cholesterol metabolism
format article
author Fan Y
Yan LT
Yao Z
Xiong GY
author_facet Fan Y
Yan LT
Yao Z
Xiong GY
author_sort Fan Y
title Biochanin A Regulates Cholesterol Metabolism Further Delays the Progression of Nonalcoholic Fatty Liver Disease
title_short Biochanin A Regulates Cholesterol Metabolism Further Delays the Progression of Nonalcoholic Fatty Liver Disease
title_full Biochanin A Regulates Cholesterol Metabolism Further Delays the Progression of Nonalcoholic Fatty Liver Disease
title_fullStr Biochanin A Regulates Cholesterol Metabolism Further Delays the Progression of Nonalcoholic Fatty Liver Disease
title_full_unstemmed Biochanin A Regulates Cholesterol Metabolism Further Delays the Progression of Nonalcoholic Fatty Liver Disease
title_sort biochanin a regulates cholesterol metabolism further delays the progression of nonalcoholic fatty liver disease
publisher Dove Medical Press
publishDate 2021
url https://doaj.org/article/a9279746a3b04a009d334bc7b721ceba
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AT yaoz biochaninaregulatescholesterolmetabolismfurtherdelaystheprogressionofnonalcoholicfattyliverdisease
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