Curcumin alleviates oxidative stress and inhibits apoptosis in diabetic cardiomyopathy via Sirt1‐Foxo1 and PI3K‐Akt signalling pathways
Diabetes is a disorder of glucose metabolism, and over 90% are type 2 diabetes. Diabetic cardiomyopathy (DCM) is one of the type 2 diabetes complications, usually accompanied by changes in myocardial structure and function, together with cardiomyocyte apoptosis. Our study investigated the effect of...
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| creator | Ren, Bin‐cheng Zhang, Yu‐fei Liu, Shan‐shan Cheng, Xiao‐jing Yang, Xin Cui, Xiao‐guang Zhao, Xin‐rui Zhao, Hui Hao, Min‐feng Li, Meng‐dan Tie, Yuan‐yuan Qu, Li Li, Xue‐yi |
| description | Diabetes is a disorder of glucose metabolism, and over 90% are type 2 diabetes. Diabetic cardiomyopathy (DCM) is one of the type 2 diabetes complications, usually accompanied by changes in myocardial structure and function, together with cardiomyocyte apoptosis. Our study investigated the effect of curcumin on regulating oxidative stress (OS) and apoptosis in DCM. In vivo, diabetes was induced in an experimental rat model by streptozoticin (STZ) together with high‐glucose and high‐fat (HG/HF) diet feeding. In vitro, H9c2 cardiomyocytes were cultured with high‐glucose and saturated free fatty acid palmitate. Curcumin was orally or directly administered to rats or cells, respectively. Streptozoticin ‐induced diabetic rats showed metabolism abnormalities and elevated markers of OS (superoxide dismutase [SOD], malondialdehyde [MDA], gp91phox, Cyt‐Cyto C), enhanced cell apoptosis (Bax/Bcl‐2, Cleaved caspase‐3, TUNEL‐positive cells), together with reduced Akt phosphorylation and increased Foxo1 acetylation. Curcumin attenuated the myocardial dysfunction, OS and apoptosis in the heart of diabetic rats. Curcumin treatment also enhanced phosphorylation of Akt and inhibited acetylation of Foxo1. These results strongly suggest that apoptosis was increased in the heart of diabetic rats, and curcumin played a role in diabetic cardiomyopathy treatment by modulating the Sirt1‐Foxo1 and PI3K‐Akt pathways. |
| doi_str_mv | 10.1111/jcmm.15725 |
| format | Article |
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Diabetic cardiomyopathy (DCM) is one of the type 2 diabetes complications, usually accompanied by changes in myocardial structure and function, together with cardiomyocyte apoptosis. Our study investigated the effect of curcumin on regulating oxidative stress (OS) and apoptosis in DCM. In vivo, diabetes was induced in an experimental rat model by streptozoticin (STZ) together with high‐glucose and high‐fat (HG/HF) diet feeding. In vitro, H9c2 cardiomyocytes were cultured with high‐glucose and saturated free fatty acid palmitate. Curcumin was orally or directly administered to rats or cells, respectively. Streptozoticin ‐induced diabetic rats showed metabolism abnormalities and elevated markers of OS (superoxide dismutase [SOD], malondialdehyde [MDA], gp91phox, Cyt‐Cyto C), enhanced cell apoptosis (Bax/Bcl‐2, Cleaved caspase‐3, TUNEL‐positive cells), together with reduced Akt phosphorylation and increased Foxo1 acetylation. Curcumin attenuated the myocardial dysfunction, OS and apoptosis in the heart of diabetic rats. Curcumin treatment also enhanced phosphorylation of Akt and inhibited acetylation of Foxo1. These results strongly suggest that apoptosis was increased in the heart of diabetic rats, and curcumin played a role in diabetic cardiomyopathy treatment by modulating the Sirt1‐Foxo1 and PI3K‐Akt pathways.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.15725</identifier><identifier>PMID: 32961025</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>1-Phosphatidylinositol 3-kinase ; Acetylation ; AKT protein ; Antibodies ; Apoptosis ; Cardiac function ; Cardiomyocytes ; Cardiomyopathy ; Caspase ; Curcumin ; Diabetes ; Diabetes mellitus (non-insulin dependent) ; Experiments ; FOXO1 protein ; Glucose ; Glucose metabolism ; High fat diet ; Kinases ; Laboratory animals ; Malondialdehyde ; Metabolism ; Original ; Oxidative stress ; Palmitic acid ; Phosphorylation ; PI3K‐Akt ; Proteins ; Signal transduction ; Sirt1 ; SIRT1 protein ; Structure-function relationships ; Superoxide dismutase ; type 2 diabetes</subject><ispartof>Journal of cellular and molecular medicine, 2020-11, Vol.24 (21), p.12355-12367</ispartof><rights>2020 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd</rights><rights>2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4485-4a456469e8fa32342ef7bd1fa06355911c63a3bc2e8592b8e2e7085ae311a1bc3</citedby><cites>FETCH-LOGICAL-c4485-4a456469e8fa32342ef7bd1fa06355911c63a3bc2e8592b8e2e7085ae311a1bc3</cites><orcidid>0000-0001-5369-872X ; 0000-0003-0990-4877</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7687015/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7687015/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32961025$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ren, Bin‐cheng</creatorcontrib><creatorcontrib>Zhang, Yu‐fei</creatorcontrib><creatorcontrib>Liu, Shan‐shan</creatorcontrib><creatorcontrib>Cheng, Xiao‐jing</creatorcontrib><creatorcontrib>Yang, Xin</creatorcontrib><creatorcontrib>Cui, Xiao‐guang</creatorcontrib><creatorcontrib>Zhao, Xin‐rui</creatorcontrib><creatorcontrib>Zhao, Hui</creatorcontrib><creatorcontrib>Hao, Min‐feng</creatorcontrib><creatorcontrib>Li, Meng‐dan</creatorcontrib><creatorcontrib>Tie, Yuan‐yuan</creatorcontrib><creatorcontrib>Qu, Li</creatorcontrib><creatorcontrib>Li, Xue‐yi</creatorcontrib><title>Curcumin alleviates oxidative stress and inhibits apoptosis in diabetic cardiomyopathy via Sirt1‐Foxo1 and PI3K‐Akt signalling pathways</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Diabetes is a disorder of glucose metabolism, and over 90% are type 2 diabetes. Diabetic cardiomyopathy (DCM) is one of the type 2 diabetes complications, usually accompanied by changes in myocardial structure and function, together with cardiomyocyte apoptosis. Our study investigated the effect of curcumin on regulating oxidative stress (OS) and apoptosis in DCM. In vivo, diabetes was induced in an experimental rat model by streptozoticin (STZ) together with high‐glucose and high‐fat (HG/HF) diet feeding. In vitro, H9c2 cardiomyocytes were cultured with high‐glucose and saturated free fatty acid palmitate. Curcumin was orally or directly administered to rats or cells, respectively. Streptozoticin ‐induced diabetic rats showed metabolism abnormalities and elevated markers of OS (superoxide dismutase [SOD], malondialdehyde [MDA], gp91phox, Cyt‐Cyto C), enhanced cell apoptosis (Bax/Bcl‐2, Cleaved caspase‐3, TUNEL‐positive cells), together with reduced Akt phosphorylation and increased Foxo1 acetylation. Curcumin attenuated the myocardial dysfunction, OS and apoptosis in the heart of diabetic rats. Curcumin treatment also enhanced phosphorylation of Akt and inhibited acetylation of Foxo1. These results strongly suggest that apoptosis was increased in the heart of diabetic rats, and curcumin played a role in diabetic cardiomyopathy treatment by modulating the Sirt1‐Foxo1 and PI3K‐Akt pathways.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Acetylation</subject><subject>AKT protein</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Cardiac function</subject><subject>Cardiomyocytes</subject><subject>Cardiomyopathy</subject><subject>Caspase</subject><subject>Curcumin</subject><subject>Diabetes</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Experiments</subject><subject>FOXO1 protein</subject><subject>Glucose</subject><subject>Glucose metabolism</subject><subject>High fat diet</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Malondialdehyde</subject><subject>Metabolism</subject><subject>Original</subject><subject>Oxidative stress</subject><subject>Palmitic acid</subject><subject>Phosphorylation</subject><subject>PI3K‐Akt</subject><subject>Proteins</subject><subject>Signal transduction</subject><subject>Sirt1</subject><subject>SIRT1 protein</subject><subject>Structure-function relationships</subject><subject>Superoxide dismutase</subject><subject>type 2 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alleviates oxidative stress and inhibits apoptosis in diabetic cardiomyopathy via Sirt1‐Foxo1 and PI3K‐Akt signalling pathways</title><author>Ren, Bin‐cheng ; Zhang, Yu‐fei ; Liu, Shan‐shan ; Cheng, Xiao‐jing ; Yang, Xin ; Cui, Xiao‐guang ; Zhao, Xin‐rui ; Zhao, Hui ; Hao, Min‐feng ; Li, Meng‐dan ; Tie, Yuan‐yuan ; Qu, Li ; Li, Xue‐yi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4485-4a456469e8fa32342ef7bd1fa06355911c63a3bc2e8592b8e2e7085ae311a1bc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Acetylation</topic><topic>AKT protein</topic><topic>Antibodies</topic><topic>Apoptosis</topic><topic>Cardiac function</topic><topic>Cardiomyocytes</topic><topic>Cardiomyopathy</topic><topic>Caspase</topic><topic>Curcumin</topic><topic>Diabetes</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Experiments</topic><topic>FOXO1 protein</topic><topic>Glucose</topic><topic>Glucose metabolism</topic><topic>High fat diet</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Malondialdehyde</topic><topic>Metabolism</topic><topic>Original</topic><topic>Oxidative stress</topic><topic>Palmitic acid</topic><topic>Phosphorylation</topic><topic>PI3K‐Akt</topic><topic>Proteins</topic><topic>Signal transduction</topic><topic>Sirt1</topic><topic>SIRT1 protein</topic><topic>Structure-function relationships</topic><topic>Superoxide dismutase</topic><topic>type 2 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ren, Bin‐cheng</creatorcontrib><creatorcontrib>Zhang, Yu‐fei</creatorcontrib><creatorcontrib>Liu, Shan‐shan</creatorcontrib><creatorcontrib>Cheng, Xiao‐jing</creatorcontrib><creatorcontrib>Yang, Xin</creatorcontrib><creatorcontrib>Cui, Xiao‐guang</creatorcontrib><creatorcontrib>Zhao, 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Bin‐cheng</au><au>Zhang, Yu‐fei</au><au>Liu, Shan‐shan</au><au>Cheng, Xiao‐jing</au><au>Yang, Xin</au><au>Cui, Xiao‐guang</au><au>Zhao, Xin‐rui</au><au>Zhao, Hui</au><au>Hao, Min‐feng</au><au>Li, Meng‐dan</au><au>Tie, Yuan‐yuan</au><au>Qu, Li</au><au>Li, Xue‐yi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Curcumin alleviates oxidative stress and inhibits apoptosis in diabetic cardiomyopathy via Sirt1‐Foxo1 and PI3K‐Akt signalling pathways</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2020-11</date><risdate>2020</risdate><volume>24</volume><issue>21</issue><spage>12355</spage><epage>12367</epage><pages>12355-12367</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Diabetes is a disorder of glucose metabolism, and over 90% are type 2 diabetes. Diabetic cardiomyopathy (DCM) is one of the type 2 diabetes complications, usually accompanied by changes in myocardial structure and function, together with cardiomyocyte apoptosis. Our study investigated the effect of curcumin on regulating oxidative stress (OS) and apoptosis in DCM. In vivo, diabetes was induced in an experimental rat model by streptozoticin (STZ) together with high‐glucose and high‐fat (HG/HF) diet feeding. In vitro, H9c2 cardiomyocytes were cultured with high‐glucose and saturated free fatty acid palmitate. Curcumin was orally or directly administered to rats or cells, respectively. Streptozoticin ‐induced diabetic rats showed metabolism abnormalities and elevated markers of OS (superoxide dismutase [SOD], malondialdehyde [MDA], gp91phox, Cyt‐Cyto C), enhanced cell apoptosis (Bax/Bcl‐2, Cleaved caspase‐3, TUNEL‐positive cells), together with reduced Akt phosphorylation and increased Foxo1 acetylation. Curcumin attenuated the myocardial dysfunction, OS and apoptosis in the heart of diabetic rats. Curcumin treatment also enhanced phosphorylation of Akt and inhibited acetylation of Foxo1. These results strongly suggest that apoptosis was increased in the heart of diabetic rats, and curcumin played a role in diabetic cardiomyopathy treatment by modulating the Sirt1‐Foxo1 and PI3K‐Akt pathways.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>32961025</pmid><doi>10.1111/jcmm.15725</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-5369-872X</orcidid><orcidid>https://orcid.org/0000-0003-0990-4877</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Wiley Online Library Open Access; DOAJ Directory of Open Access Journals; Wiley Online Library Journals Frontfile Complete; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | 1-Phosphatidylinositol 3-kinase Acetylation AKT protein Antibodies Apoptosis Cardiac function Cardiomyocytes Cardiomyopathy Caspase Curcumin Diabetes Diabetes mellitus (non-insulin dependent) Experiments FOXO1 protein Glucose Glucose metabolism High fat diet Kinases Laboratory animals Malondialdehyde Metabolism Original Oxidative stress Palmitic acid Phosphorylation PI3K‐Akt Proteins Signal transduction Sirt1 SIRT1 protein Structure-function relationships Superoxide dismutase type 2 diabetes |
| title | Curcumin alleviates oxidative stress and inhibits apoptosis in diabetic cardiomyopathy via Sirt1‐Foxo1 and PI3K‐Akt signalling pathways |
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