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 inJournal of cellular and molecular medicine Vol. 24; no. 21; pp. 12355 - 12367
Main Authors 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
Format Journal Article
LanguageEnglish
Published England John Wiley & Sons, Inc 01.11.2020
John Wiley and Sons Inc
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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.
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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2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
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Issue 21
Keywords apoptosis
Sirt1
type 2 diabetes
PI3K-Akt
oxidative stress
curcumin
Language English
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2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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This work was supported by the National Natural Science Foundation of China (NSFC), No. 81373200.
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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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StartPage 12355
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
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjcmm.15725
https://www.ncbi.nlm.nih.gov/pubmed/32961025
https://www.proquest.com/docview/2463936180
https://www.proquest.com/docview/2445429895
https://pubmed.ncbi.nlm.nih.gov/PMC7687015
Volume 24
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