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The antioxidant edaravone prevents cardiac dysfunction by suppressing oxidative stress in type 1 diabetic rats and in high-glucose-induced injured H9c2 cardiomyoblasts.
Can J Physiol Pharmacol. 2016 Sep; 94(9):996-1006.CJ

Abstract

Edaravone, a radical scavenger, has been recognized as a potential protective agent for cardiovascular diseases. However, little is known about the effect of edaravone in cardiac complications associated with diabetes. Here, we have demonstrated that edaravone prevents cardiac dysfunction and apoptosis in the streptozotocin-induced type 1 diabetic rat heart. Mechanistic studies revealed that edaravone treatment improved cardiac function and restored superoxide dismutase levels. In addition, treatment of diabetic animals by edaravone increased protein expressions of sirtuin-1 (SIRT-1), peroxisome proliferator activated receptor γ coactivator α (PGC-1α), nuclear factor like-2 (NRF-2), and B cell lymphoma 2 (Bcl-2), and reduced protein expressions of Bax and Caspase-3 compared to the control group. High glucose incubation resulted in the production of reactive oxygen species (ROS) and cell death. Treatment of high-glucose-incubated H9c2 cells by edaravone reduced ROS production and cell death. In addition, the treatment of high-glucose-incubated H9c2 cells by edaravone increased the activity of antioxidative stress by increasing SIRT-1, PGC-1α, and NRF-2, and this treatment also reduced apoptosis by increasing Bcl-2 expression and reducing Bax and Caspase-3 expressions. Knockdown SIRT-1 with small interferer RNA abolished the effects of edaravone. Overall, our data demonstrated that edaravone may be an effective agent against the development of diabetic cardiomyopathy.

Authors+Show Affiliations

a Department of Cardiology, First Hospital of Jilin University, Changchun 130021, China. b Department of Cardiology, Changchun Central Hospital, Changchun 130051, China.c Department of Nephrology, China-Japan Union Hospital of Jilin University, Changchun 130033, China.d Department of Neurology, First Hospital of Jilin University, Changchun 130021, China.e Department of Pharmacology, College of Basic Medical Sciences, Jilin University, Changchun 130021, China.b Department of Cardiology, Changchun Central Hospital, Changchun 130051, China.e Department of Pharmacology, College of Basic Medical Sciences, Jilin University, Changchun 130021, China.b Department of Cardiology, Changchun Central Hospital, Changchun 130051, China.a Department of Cardiology, First Hospital of Jilin University, Changchun 130021, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27376621

Citation

Ji, Lei, et al. "The Antioxidant Edaravone Prevents Cardiac Dysfunction By Suppressing Oxidative Stress in Type 1 Diabetic Rats and in High-glucose-induced Injured H9c2 Cardiomyoblasts." Canadian Journal of Physiology and Pharmacology, vol. 94, no. 9, 2016, pp. 996-1006.
Ji L, Liu Y, Zhang Y, et al. The antioxidant edaravone prevents cardiac dysfunction by suppressing oxidative stress in type 1 diabetic rats and in high-glucose-induced injured H9c2 cardiomyoblasts. Can J Physiol Pharmacol. 2016;94(9):996-1006.
Ji, L., Liu, Y., Zhang, Y., Chang, W., Gong, J., Wei, S., Li, X., & Qin, L. (2016). The antioxidant edaravone prevents cardiac dysfunction by suppressing oxidative stress in type 1 diabetic rats and in high-glucose-induced injured H9c2 cardiomyoblasts. Canadian Journal of Physiology and Pharmacology, 94(9), 996-1006. https://doi.org/10.1139/cjpp-2015-0587
Ji L, et al. The Antioxidant Edaravone Prevents Cardiac Dysfunction By Suppressing Oxidative Stress in Type 1 Diabetic Rats and in High-glucose-induced Injured H9c2 Cardiomyoblasts. Can J Physiol Pharmacol. 2016;94(9):996-1006. PubMed PMID: 27376621.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The antioxidant edaravone prevents cardiac dysfunction by suppressing oxidative stress in type 1 diabetic rats and in high-glucose-induced injured H9c2 cardiomyoblasts. AU - Ji,Lei, AU - Liu,Yingying, AU - Zhang,Ying, AU - Chang,Wenguang, AU - Gong,Junli, AU - Wei,Shengnan, AU - Li,Xudong, AU - Qin,Ling, Y1 - 2016/05/18/ PY - 2016/7/5/entrez PY - 2016/7/5/pubmed PY - 2017/5/24/medline KW - apoptose KW - apoptosis KW - diabète de type 1 KW - edaravone KW - oxidative stress KW - stress oxydatif KW - type 1 diabetes KW - édaravone SP - 996 EP - 1006 JF - Canadian journal of physiology and pharmacology JO - Can J Physiol Pharmacol VL - 94 IS - 9 N2 - Edaravone, a radical scavenger, has been recognized as a potential protective agent for cardiovascular diseases. However, little is known about the effect of edaravone in cardiac complications associated with diabetes. Here, we have demonstrated that edaravone prevents cardiac dysfunction and apoptosis in the streptozotocin-induced type 1 diabetic rat heart. Mechanistic studies revealed that edaravone treatment improved cardiac function and restored superoxide dismutase levels. In addition, treatment of diabetic animals by edaravone increased protein expressions of sirtuin-1 (SIRT-1), peroxisome proliferator activated receptor γ coactivator α (PGC-1α), nuclear factor like-2 (NRF-2), and B cell lymphoma 2 (Bcl-2), and reduced protein expressions of Bax and Caspase-3 compared to the control group. High glucose incubation resulted in the production of reactive oxygen species (ROS) and cell death. Treatment of high-glucose-incubated H9c2 cells by edaravone reduced ROS production and cell death. In addition, the treatment of high-glucose-incubated H9c2 cells by edaravone increased the activity of antioxidative stress by increasing SIRT-1, PGC-1α, and NRF-2, and this treatment also reduced apoptosis by increasing Bcl-2 expression and reducing Bax and Caspase-3 expressions. Knockdown SIRT-1 with small interferer RNA abolished the effects of edaravone. Overall, our data demonstrated that edaravone may be an effective agent against the development of diabetic cardiomyopathy. SN - 1205-7541 UR - https://www.unboundmedicine.com/medline/citation/27376621/The_antioxidant_edaravone_prevents_cardiac_dysfunction_by_suppressing_oxidative_stress_in_type_1_diabetic_rats_and_in_high_glucose_induced_injured_H9c2_cardiomyoblasts_ L2 - https://cdnsciencepub.com/doi/10.1139/cjpp-2015-0587?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -