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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Published in | Journal of cellular and molecular medicine Vol. 24; no. 21; pp. 12355 - 12367 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
John Wiley & Sons, Inc
01.11.2020
John Wiley and Sons Inc |
Subjects | |
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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. |
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AbstractList | 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], gp91
, 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. 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. 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], gp91 phox , 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. 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.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. |
Author | Ren, Bin‐cheng Yang, Xin Liu, Shan‐shan Cheng, Xiao‐jing Cui, Xiao‐guang Zhao, Hui Qu, Li Tie, Yuan‐yuan Zhang, Yu‐fei Li, Xue‐yi Zhao, Xin‐rui Hao, Min‐feng Li, Meng‐dan |
AuthorAffiliation | 2 State Key Laboratory of Crop Stress Biology for Arid Areas and College of Life Sciences Northwest A&F University Yangling China 1 Department of Rheumatology and Immunology Second Affiliated Hospital of Xi'an Jiaotong University Xi'an China 3 Department of Neurology Xi'an Central Hospital Xi'an China 4 Department of Cardiovascular Medicine Second Affiliated Hospital of Xi'an Jiaotong University Xi'an China |
AuthorAffiliation_xml | – name: 2 State Key Laboratory of Crop Stress Biology for Arid Areas and College of Life Sciences Northwest A&F University Yangling China – name: 3 Department of Neurology Xi'an Central Hospital Xi'an China – name: 1 Department of Rheumatology and Immunology Second Affiliated Hospital of Xi'an Jiaotong University Xi'an China – name: 4 Department of Cardiovascular Medicine Second Affiliated Hospital of Xi'an Jiaotong University Xi'an China |
Author_xml | – sequence: 1 givenname: Bin‐cheng surname: Ren fullname: Ren, Bin‐cheng organization: Second Affiliated Hospital of Xi'an Jiaotong University – sequence: 2 givenname: Yu‐fei orcidid: 0000-0001-5369-872X surname: Zhang fullname: Zhang, Yu‐fei organization: Northwest A&F University – sequence: 3 givenname: Shan‐shan surname: Liu fullname: Liu, Shan‐shan organization: Second Affiliated Hospital of Xi'an Jiaotong University – sequence: 4 givenname: Xiao‐jing surname: Cheng fullname: Cheng, Xiao‐jing organization: Second Affiliated Hospital of Xi'an Jiaotong University – sequence: 5 givenname: Xin surname: Yang fullname: Yang, Xin organization: Second Affiliated Hospital of Xi'an Jiaotong University – sequence: 6 givenname: Xiao‐guang surname: Cui fullname: Cui, Xiao‐guang organization: Second Affiliated Hospital of Xi'an Jiaotong University – sequence: 7 givenname: Xin‐rui surname: Zhao fullname: Zhao, Xin‐rui organization: Second Affiliated Hospital of Xi'an Jiaotong University – sequence: 8 givenname: Hui surname: Zhao fullname: Zhao, Hui organization: Second Affiliated Hospital of Xi'an Jiaotong University – sequence: 9 givenname: Min‐feng surname: Hao fullname: Hao, Min‐feng organization: Xi'an Central Hospital – sequence: 10 givenname: Meng‐dan surname: Li fullname: Li, Meng‐dan organization: Second Affiliated Hospital of Xi'an Jiaotong University – sequence: 11 givenname: Yuan‐yuan orcidid: 0000-0003-0990-4877 surname: Tie fullname: Tie, Yuan‐yuan organization: Second Affiliated Hospital of Xi'an Jiaotong University – sequence: 12 givenname: Li surname: Qu fullname: Qu, Li organization: Second Affiliated Hospital of Xi'an Jiaotong University – sequence: 13 givenname: Xue‐yi surname: Li fullname: Li, Xue‐yi email: 13992891987@139.com organization: Second Affiliated Hospital of Xi'an Jiaotong University |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32961025$$D View this record in MEDLINE/PubMed |
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Copyright | 2020 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. 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. |
Copyright_xml | – notice: 2020 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd – notice: 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. – notice: 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. |
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DOI | 10.1111/jcmm.15725 |
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Keywords | apoptosis Sirt1 type 2 diabetes PI3K-Akt oxidative stress curcumin |
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Snippet | 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,... |
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SubjectTerms | 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 |
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Title | Curcumin alleviates oxidative stress and inhibits apoptosis in diabetic cardiomyopathy via Sirt1‐Foxo1 and PI3K‐Akt signalling pathways |
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