Abstract Title:

Cinnamaldehyde Ameliorates High-Glucose-Induced Oxidative Stress and Cardiomyocyte Injury Through Transient Receptor Potential Ankyrin 1.

Abstract Source:

J Cardiovasc Pharmacol. 2019 Jul ;74(1):30-37. PMID: 31274840

Abstract Author(s):

Dan Wang, Jixin Hou, Yi Yang, Peng Zhou, Sen Liu, Jindong Wan, Peijian Wang

Article Affiliation:

Dan Wang


Oxidative stress plays a critical role in diabetic cardiomyopathy. Transient receptor potential ankyrin subtype 1 (TRPA1) has antioxidative property. In this study, we tested whether activation of TRPA1 with cinnamaldehyde protects against high-glucose-induced cardiomyocyte injury. Cinnamaldehyde remarkably decreased high-glucose-induced mitochondrial superoxide overproduction, upregulation of nitrotyrosine, P22, and P47, and apoptosis in cultured H9C2 cardiomyocytes (P<0.01), which were abolished by a TRPA1 antagonist HC030031 (P<0.01). Nrf2 and its induced genes heme oxygenase-1 (HO-1), glutathione peroxidase-1 (GPx-1), and quinone oxidoreductase-1 (NQO-1) were slightly increased by high glucose (P<0.01) and further upregulated by cinnamaldehyde (P<0.05 or P<0.01). Feeding with cinnamaldehyde (0.02%)-containing diet for 12 weeks significantly decreased cardiac nitrotyrosine levels (P<0.01), fibrosis, and cardiomyocyte hypertrophy (P<0.05), while increased expression of antioxidative enzymes (HO-1, GPx-1, NQO-1, and catalase) (P<0.01) in the myocardial tissue of db/db diabetic mice. These results suggest that cinnamaldehyde protects against high-glucose-induced oxidative damage of cardiomyocytes likely through the TRPA1/Nrf2 pathway.

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