Oral flavonoid fisetin treatment protects against prolonged high-fat-diet-induced cardiac dysfunction by regulation of multicombined signaling
Excess high-fat diet (HFD) intake predisposes the occurrence of obesity-associated heart injury, but the mechanism is elusive. Fisetin (FIS), as a natural flavonoid, has potential activities to alleviate obesity-induced metabolic syndrome. However, the underlying molecular mechanisms of FIS against...
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| creator | Hu, Lin-Feng Feng, Jing Dai, Xianling Sun, Yan Xiong, Mingxin Lai, Lili Zhong, Shaoyu Yi, Chao Chen, Geng Li, Huanhuan Yang, Qiufeng Kuang, Qin Long, Tingting Zhan, Jianxia Tang, Tingting Ge, Chenxu Tan, Jun Xu, Minxuan |
| description | Excess high-fat diet (HFD) intake predisposes the occurrence of obesity-associated heart injury, but the mechanism is elusive. Fisetin (FIS), as a natural flavonoid, has potential activities to alleviate obesity-induced metabolic syndrome. However, the underlying molecular mechanisms of FIS against HFD-induced cardiac injury remain unclear. The present study was to explore the protective effects of FIS on cardiac dysfunction in HFD-fed mice. We found that FIS alleviated HFD-triggered metabolic disorder by reducing body weight, fasting blood glucose and insulin levels, and insulin resistance. Moreover, FIS supplements significantly alleviated dyslipidemia in both mouse hearts and cardiomyocytes stimulated by metabolic stress. FIS treatment abolished HFD-induced inflammatory response in heart tissues through suppressing TNF receptor-1/TNF receptor-associated factor-2 (Tnfr-1/Traf-2) signaling. Furthermore, FIS induced a strong reduction in the expression of fibrosis-related genes, contributing to the inhibition of fibrosis by inactivating transforming growth factor (Tgf)-β1/Smads/Erk1/2 signaling. Collectively, these results demonstrated that FIS could be a promising therapeutic strategy for the treatment of obesity-associated cardiac injury. |
| doi_str_mv | 10.1016/j.jnutbio.2019.108253 |
| format | Article |
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Fisetin (FIS), as a natural flavonoid, has potential activities to alleviate obesity-induced metabolic syndrome. However, the underlying molecular mechanisms of FIS against HFD-induced cardiac injury remain unclear. The present study was to explore the protective effects of FIS on cardiac dysfunction in HFD-fed mice. We found that FIS alleviated HFD-triggered metabolic disorder by reducing body weight, fasting blood glucose and insulin levels, and insulin resistance. Moreover, FIS supplements significantly alleviated dyslipidemia in both mouse hearts and cardiomyocytes stimulated by metabolic stress. FIS treatment abolished HFD-induced inflammatory response in heart tissues through suppressing TNF receptor-1/TNF receptor-associated factor-2 (Tnfr-1/Traf-2) signaling. Furthermore, FIS induced a strong reduction in the expression of fibrosis-related genes, contributing to the inhibition of fibrosis by inactivating transforming growth factor (Tgf)-β1/Smads/Erk1/2 signaling. Collectively, these results demonstrated that FIS could be a promising therapeutic strategy for the treatment of obesity-associated cardiac injury.</description><identifier>ISSN: 0955-2863</identifier><identifier>EISSN: 1873-4847</identifier><identifier>DOI: 10.1016/j.jnutbio.2019.108253</identifier><identifier>PMID: 31835147</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Diet, High-Fat ; Disease Models, Animal ; Dyslipidemias - drug therapy ; Dyslipidemias - metabolism ; Echocardiography ; Fibrosis ; Fisetin ; Flavonoids - pharmacology ; Glucose Tolerance Test ; Heart - drug effects ; Heart - physiology ; Heart Diseases - drug therapy ; Heart Diseases - metabolism ; Inflammation ; Insulin - metabolism ; Insulin Resistance ; Insulin resistance and dyslipidemia ; Male ; Metabolic syndrome ; Metabolic Syndrome - drug therapy ; Metabolic Syndrome - metabolism ; Mice ; Mice, Inbred C57BL ; Myocardium - metabolism ; Myocytes, Cardiac - metabolism ; Rats ; Rats, Wistar ; Signal Transduction ; Tgf-β1/Smads/Erk1/2 ; Tnfr-1/Traf-2</subject><ispartof>The Journal of nutritional biochemistry, 2020-03, Vol.77, p.108253-108253, Article 108253</ispartof><rights>2019 Elsevier Inc.</rights><rights>Copyright © 2019 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c365t-d3cfcb0a7e2cae0fe3573eca9b80c51ab04c9c8e1eea92babea75689ead9841e3</citedby><cites>FETCH-LOGICAL-c365t-d3cfcb0a7e2cae0fe3573eca9b80c51ab04c9c8e1eea92babea75689ead9841e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0955286319301408$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31835147$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hu, Lin-Feng</creatorcontrib><creatorcontrib>Feng, Jing</creatorcontrib><creatorcontrib>Dai, Xianling</creatorcontrib><creatorcontrib>Sun, Yan</creatorcontrib><creatorcontrib>Xiong, Mingxin</creatorcontrib><creatorcontrib>Lai, Lili</creatorcontrib><creatorcontrib>Zhong, Shaoyu</creatorcontrib><creatorcontrib>Yi, Chao</creatorcontrib><creatorcontrib>Chen, Geng</creatorcontrib><creatorcontrib>Li, Huanhuan</creatorcontrib><creatorcontrib>Yang, Qiufeng</creatorcontrib><creatorcontrib>Kuang, Qin</creatorcontrib><creatorcontrib>Long, Tingting</creatorcontrib><creatorcontrib>Zhan, Jianxia</creatorcontrib><creatorcontrib>Tang, Tingting</creatorcontrib><creatorcontrib>Ge, Chenxu</creatorcontrib><creatorcontrib>Tan, Jun</creatorcontrib><creatorcontrib>Xu, Minxuan</creatorcontrib><title>Oral flavonoid fisetin treatment protects against prolonged high-fat-diet-induced cardiac dysfunction by regulation of multicombined signaling</title><title>The Journal of nutritional biochemistry</title><addtitle>J Nutr Biochem</addtitle><description>Excess high-fat diet (HFD) intake predisposes the occurrence of obesity-associated heart injury, but the mechanism is elusive. Fisetin (FIS), as a natural flavonoid, has potential activities to alleviate obesity-induced metabolic syndrome. However, the underlying molecular mechanisms of FIS against HFD-induced cardiac injury remain unclear. The present study was to explore the protective effects of FIS on cardiac dysfunction in HFD-fed mice. We found that FIS alleviated HFD-triggered metabolic disorder by reducing body weight, fasting blood glucose and insulin levels, and insulin resistance. Moreover, FIS supplements significantly alleviated dyslipidemia in both mouse hearts and cardiomyocytes stimulated by metabolic stress. FIS treatment abolished HFD-induced inflammatory response in heart tissues through suppressing TNF receptor-1/TNF receptor-associated factor-2 (Tnfr-1/Traf-2) signaling. Furthermore, FIS induced a strong reduction in the expression of fibrosis-related genes, contributing to the inhibition of fibrosis by inactivating transforming growth factor (Tgf)-β1/Smads/Erk1/2 signaling. Collectively, these results demonstrated that FIS could be a promising therapeutic strategy for the treatment of obesity-associated cardiac injury.</description><subject>Animals</subject><subject>Diet, High-Fat</subject><subject>Disease Models, Animal</subject><subject>Dyslipidemias - drug therapy</subject><subject>Dyslipidemias - metabolism</subject><subject>Echocardiography</subject><subject>Fibrosis</subject><subject>Fisetin</subject><subject>Flavonoids - pharmacology</subject><subject>Glucose Tolerance Test</subject><subject>Heart - drug effects</subject><subject>Heart - physiology</subject><subject>Heart Diseases - drug therapy</subject><subject>Heart Diseases - metabolism</subject><subject>Inflammation</subject><subject>Insulin - metabolism</subject><subject>Insulin Resistance</subject><subject>Insulin resistance and dyslipidemia</subject><subject>Male</subject><subject>Metabolic syndrome</subject><subject>Metabolic Syndrome - drug therapy</subject><subject>Metabolic Syndrome - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Myocardium - metabolism</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Signal Transduction</subject><subject>Tgf-β1/Smads/Erk1/2</subject><subject>Tnfr-1/Traf-2</subject><issn>0955-2863</issn><issn>1873-4847</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUcFu1TAQtBCIvhY-AeQjlzzsOE6cE0IVUKRKvcDZ2jibdJ8Su9hOpfcTfDNu34Mrp9WOZna0M4y9k2IvhWw_HvYHv-WBwr4Wsi-YqbV6wXbSdKpqTNO9ZDvRa13VplUX7DKlgxCibnT7ml0oaZSWTbdjv-8iLHxa4DH4QCOfKGEmz3NEyCv6zB9iyOhy4jAD-fQMLMHPOPJ7mu-rCXI1EuaK_Li5gjqII4Hj4zFNm3eZgufDkUectwWetzDxdVsyubAO5Isk0exhIT-_Ya8mWBK-Pc8r9vPrlx_XN9Xt3bfv159vK6daXfyUm9wgoMPaAYoJle4UOugHI5yWMIjG9c6gRIS-HmBA6HRreoSxN41EdcU-nO6WZ35tmLJdKTlcFvAYtmRrVXeqk0KbQtUnqoshpYiTfYi0QjxaKexTFfZgz1XYpyrsqYqie3-22IYVx3-qv9kXwqcTAcujj4TRJkfoS4QUS-B2DPQfiz-wCKMC</recordid><startdate>202003</startdate><enddate>202003</enddate><creator>Hu, Lin-Feng</creator><creator>Feng, Jing</creator><creator>Dai, Xianling</creator><creator>Sun, Yan</creator><creator>Xiong, Mingxin</creator><creator>Lai, Lili</creator><creator>Zhong, Shaoyu</creator><creator>Yi, Chao</creator><creator>Chen, Geng</creator><creator>Li, Huanhuan</creator><creator>Yang, Qiufeng</creator><creator>Kuang, Qin</creator><creator>Long, Tingting</creator><creator>Zhan, Jianxia</creator><creator>Tang, Tingting</creator><creator>Ge, Chenxu</creator><creator>Tan, Jun</creator><creator>Xu, Minxuan</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>202003</creationdate><title>Oral flavonoid fisetin treatment protects against prolonged high-fat-diet-induced cardiac dysfunction by regulation of multicombined signaling</title><author>Hu, Lin-Feng ; 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Fisetin (FIS), as a natural flavonoid, has potential activities to alleviate obesity-induced metabolic syndrome. However, the underlying molecular mechanisms of FIS against HFD-induced cardiac injury remain unclear. The present study was to explore the protective effects of FIS on cardiac dysfunction in HFD-fed mice. We found that FIS alleviated HFD-triggered metabolic disorder by reducing body weight, fasting blood glucose and insulin levels, and insulin resistance. Moreover, FIS supplements significantly alleviated dyslipidemia in both mouse hearts and cardiomyocytes stimulated by metabolic stress. FIS treatment abolished HFD-induced inflammatory response in heart tissues through suppressing TNF receptor-1/TNF receptor-associated factor-2 (Tnfr-1/Traf-2) signaling. Furthermore, FIS induced a strong reduction in the expression of fibrosis-related genes, contributing to the inhibition of fibrosis by inactivating transforming growth factor (Tgf)-β1/Smads/Erk1/2 signaling. Collectively, these results demonstrated that FIS could be a promising therapeutic strategy for the treatment of obesity-associated cardiac injury.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>31835147</pmid><doi>10.1016/j.jnutbio.2019.108253</doi><tpages>1</tpages></addata></record> |
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| subjects | Animals Diet, High-Fat Disease Models, Animal Dyslipidemias - drug therapy Dyslipidemias - metabolism Echocardiography Fibrosis Fisetin Flavonoids - pharmacology Glucose Tolerance Test Heart - drug effects Heart - physiology Heart Diseases - drug therapy Heart Diseases - metabolism Inflammation Insulin - metabolism Insulin Resistance Insulin resistance and dyslipidemia Male Metabolic syndrome Metabolic Syndrome - drug therapy Metabolic Syndrome - metabolism Mice Mice, Inbred C57BL Myocardium - metabolism Myocytes, Cardiac - metabolism Rats Rats, Wistar Signal Transduction Tgf-β1/Smads/Erk1/2 Tnfr-1/Traf-2 |
| title | Oral flavonoid fisetin treatment protects against prolonged high-fat-diet-induced cardiac dysfunction by regulation of multicombined signaling |
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