Tags

Type your tag names separated by a space and hit enter

Taxifolin prevents diabetic cardiomyopathy in vivo and in vitro by inhibition of oxidative stress and cell apoptosis.
Food Chem Toxicol 2014; 63:221-32FC

Abstract

Diabetic cardiomyopathy has been increasingly recognized as an important cause of heart failure in diabetic patients. Excessive oxidative stress has been suggested to play a critical role in the development of diabetic cardiomyopathy. The objective of this study was to investigate the potential protective effects and mechanisms of taxifolin on cardiac function of streptozotocin-induced diabetic mice and on hyperglycemia-induced apoptosis of H9c2 cardiac myoblasts. In vivo study revealed that taxifolin improved diastolic dysfunction, ameliorated myocardium structure abnormality, inhibited myocyte apoptosis and enhanced endogenous antioxidant enzymes activities. Interestingly, taxifolin reduced angiotensin II level in myocardium, inhibited NADPH oxidase activity, and increased JAK/STAT3 activation. In vitro investigation demonstrated that taxifolin inhibited 33 mM glucoseinduced H9c2 cells apoptosis by decreasing intracellular ROS level. It also inhibited caspase-3 and caspase-9 activation, restored mitochondrial membrane potential, and regulated the expression of proteins related to the intrinsic pathway of apoptosis, thus inhibiting the release of cytochrome c from mitochondria into the cytoplasm. In conclusion, taxifolin exerted cardioprotective effects against diabetic cardiomyopathy by inhibiting oxidative stress and cardiac myocyte apoptosis and might be a potential agent in the treatment of diabetic cardiomyopathy.

Authors+Show Affiliations

Key Laboratory of Bioactive Substances and Resources Utilization of Chinese Herbal Medicine, Institute of Medicinal Plant Development (IMPLAD), Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.Key Laboratory of Bioactive Substances and Resources Utilization of Chinese Herbal Medicine, Institute of Medicinal Plant Development (IMPLAD), Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.Key Laboratory of Bioactive Substances and Resources Utilization of Chinese Herbal Medicine, Institute of Medicinal Plant Development (IMPLAD), Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.Key Laboratory of Bioactive Substances and Resources Utilization of Chinese Herbal Medicine, Institute of Medicinal Plant Development (IMPLAD), Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.Key Laboratory of Bioactive Substances and Resources Utilization of Chinese Herbal Medicine, Institute of Medicinal Plant Development (IMPLAD), Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.Key Laboratory of Bioactive Substances and Resources Utilization of Chinese Herbal Medicine, Institute of Medicinal Plant Development (IMPLAD), Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.Medical Functional Laboratory, Basic Medical Department, Beihua University, Jilin, China.Key Laboratory of Bioactive Substances and Resources Utilization of Chinese Herbal Medicine, Institute of Medicinal Plant Development (IMPLAD), Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China. Electronic address: sunxiaobosubmit@163.com.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24269735

Citation

Sun, Xiao, et al. "Taxifolin Prevents Diabetic Cardiomyopathy in Vivo and in Vitro By Inhibition of Oxidative Stress and Cell Apoptosis." Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association, vol. 63, 2014, pp. 221-32.
Sun X, Chen RC, Yang ZH, et al. Taxifolin prevents diabetic cardiomyopathy in vivo and in vitro by inhibition of oxidative stress and cell apoptosis. Food Chem Toxicol. 2014;63:221-32.
Sun, X., Chen, R. C., Yang, Z. H., Sun, G. B., Wang, M., Ma, X. J., ... Sun, X. B. (2014). Taxifolin prevents diabetic cardiomyopathy in vivo and in vitro by inhibition of oxidative stress and cell apoptosis. Food and Chemical Toxicology : an International Journal Published for the British Industrial Biological Research Association, 63, pp. 221-32. doi:10.1016/j.fct.2013.11.013.
Sun X, et al. Taxifolin Prevents Diabetic Cardiomyopathy in Vivo and in Vitro By Inhibition of Oxidative Stress and Cell Apoptosis. Food Chem Toxicol. 2014;63:221-32. PubMed PMID: 24269735.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Taxifolin prevents diabetic cardiomyopathy in vivo and in vitro by inhibition of oxidative stress and cell apoptosis. AU - Sun,Xiao, AU - Chen,Rong-chang, AU - Yang,Zhi-hong, AU - Sun,Gui-bo, AU - Wang,Min, AU - Ma,Xiao-jun, AU - Yang,Li-juan, AU - Sun,Xiao-bo, Y1 - 2013/11/20/ PY - 2013/07/23/received PY - 2013/11/05/revised PY - 2013/11/11/accepted PY - 2013/11/26/entrez PY - 2013/11/26/pubmed PY - 2014/9/23/medline KW - AST KW - AT1 KW - Ang II KW - Apoptosis KW - CAT KW - CK-MB KW - DCM KW - Diabetic cardiomyopathy KW - EF KW - FS KW - GSH-Px KW - LDH KW - LV end-diastolic volume KW - LV end-systolic volume KW - LVVd KW - LVVs KW - MDA KW - NADPH oxidase KW - Oxidative stress KW - RAS KW - ROS KW - SOD KW - STZ KW - Taxifolin KW - angiotensin II KW - angiotensin receptor 1 KW - aspartate aminotransferase KW - catalase KW - creatinine kinase-MB isoenzyme KW - diabetic cardiomyopathy KW - ejection fraction KW - fractional shortening KW - glutathione peroxidase KW - lactate dehydrogenase KW - malondialdehyde KW - mitochondrial membrane potential KW - reactive oxygen species KW - rennin-angiotensin system KW - streptozotocin KW - superoxide dismutase KW - ΔΨ(m) SP - 221 EP - 32 JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association JO - Food Chem. Toxicol. VL - 63 N2 - Diabetic cardiomyopathy has been increasingly recognized as an important cause of heart failure in diabetic patients. Excessive oxidative stress has been suggested to play a critical role in the development of diabetic cardiomyopathy. The objective of this study was to investigate the potential protective effects and mechanisms of taxifolin on cardiac function of streptozotocin-induced diabetic mice and on hyperglycemia-induced apoptosis of H9c2 cardiac myoblasts. In vivo study revealed that taxifolin improved diastolic dysfunction, ameliorated myocardium structure abnormality, inhibited myocyte apoptosis and enhanced endogenous antioxidant enzymes activities. Interestingly, taxifolin reduced angiotensin II level in myocardium, inhibited NADPH oxidase activity, and increased JAK/STAT3 activation. In vitro investigation demonstrated that taxifolin inhibited 33 mM glucoseinduced H9c2 cells apoptosis by decreasing intracellular ROS level. It also inhibited caspase-3 and caspase-9 activation, restored mitochondrial membrane potential, and regulated the expression of proteins related to the intrinsic pathway of apoptosis, thus inhibiting the release of cytochrome c from mitochondria into the cytoplasm. In conclusion, taxifolin exerted cardioprotective effects against diabetic cardiomyopathy by inhibiting oxidative stress and cardiac myocyte apoptosis and might be a potential agent in the treatment of diabetic cardiomyopathy. SN - 1873-6351 UR - https://www.unboundmedicine.com/medline/citation/24269735/Taxifolin_prevents_diabetic_cardiomyopathy_in_vivo_and_in_vitro_by_inhibition_of_oxidative_stress_and_cell_apoptosis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0278-6915(13)00758-8 DB - PRIME DP - Unbound Medicine ER -