期刊
JOURNAL OF MEDICINAL FOOD
卷 18, 期 7, 页码 793-801出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/jmf.2014.3342
关键词
diabetes; gallic acid; proinflammatory cytokine; center dot epigenetics
资金
- Basic Science Research Program through National Research Foundation of Korea (NRF) - Ministry of Education [2014R1A1A2059288]
- National Research Foundation of Korea [2014R1A1A2059288] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Hyperglycemia contributes to diabetes and several diabetes-related complications. Gallic acid is a polyhydroxy phenolic compound found in various natural products. In this study, we investigated the effects and mechanism of gallic acid on proinflammatory cytokine secretion in high glucose-induced human monocytes (THP-1 cells). THP-1 cells were cultured under normoglycemic or hyperglycemic conditions, in the absence or presence of gallic acid. Hyperglycemic conditions significantly induced histone acetylation, nuclear factor-kappa B (NF-kappa B) activation, and proinflammatory cytokine release from THP-1 cells, whereas gallic acid suppressed NF-kappa B activity and cytokine release. It also significantly reduced CREB-binding protein/p300 (CBP/p300, a NF-kappa B coactivator) gene expression, acetylation levels, and CBP/p300 histone acetyltransferase (HAT) activity. In addition, histone deacetylase 2 (HDAC2) expression was significantly induced. These results suggest that gallic acid inhibits hyperglycemic-induced cytokine production in monocytes through epigenetic changes involving NF-kappa B. Therefore, gallic acid may have potential for the treatment and prevention of diabetes and its complications.
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