Abstract:
: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.
journal_name
J Cardiovasc Pharmacoljournal_title
Journal of cardiovascular pharmacologyauthors
Wang D,Hou J,Yang Y,Zhou P,Liu S,Wan J,Wang Pdoi
10.1097/FJC.0000000000000679subject
Has Abstractpub_date
2019-07-01 00:00:00pages
30-37issue
1eissn
0160-2446issn
1533-4023pii
00005344-201907000-00006journal_volume
74pub_type
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