title: Gallic Acid Decreases Inflammatory Cytokine Secretion Through Histone Acetyltransferase/Histone Deacetylase Regulation in High Glucose-Induced Human Monocytes.
abstract: 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-κB (NF-κB) activation, and proinflammatory cytokine release from THP-1 cells, whereas gallic acid suppressed NF-κB activity and cytokine release. It also significantly reduced CREB-binding protein/p300 (CBP/p300, a NF-κB 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-κB. Therefore, gallic acid may have potential for the treatment and prevention of diabetes and its complications.
authors: 1 Samsung Advanced Institute for Health Science & Technology, Samsung Medical Center , Seoul, South Korea .
authors: Wooje
authors: W
authors: Lee
authors: 2 Department of Life Science, Gachon University , Kyeonggi, South Korea .
authors: Sang Yeol
authors: SY
authors: Lee
authors: 3 Department of Pharmacy, Sunchon National University , Sunchon, Jeonnam, South Korea .
authors: Young-Jin
authors: YJ
authors: Son
authors: 4 Department of Food and Nutrition, Chonnam National University , Gwangju, South Korea .
authors: Jung-Mi
authors: JM
authors: Yun
mesh_terms: D000107:Acetylation; D050882:CREB-Binding Protein / Q000235:genetics / Q000378:metabolism; D002460:Cell Line; D016207:Cytokines / Q000378:metabolism*; D044127:Epigenesis, Genetic; D005707:Gallic Acid / Q000494:pharmacology*; D015870:Gene Expression / Q000187:drug effects; D005947:Glucose / Q000494:pharmacology*; D051548:Histone Acetyltransferases / Q000378:metabolism*; D006655:Histone Deacetylases / Q000378:metabolism*; D006801:Humans; D006943:Hyperglycemia; D007249:Inflammation; D009000:Monocytes / Q000187:drug effects* / Q000502:physiology; D016328:NF-kappa B / Q000037:antagonists & inhibitors; D050880:p300-CBP Transcription Factors / Q000235:genetics / Q000378:metabolism
chemical_list: D016207:Cytokines; D016328:NF-kappa B; D005707:Gallic Acid; D050882:CREB-Binding Protein; C494363:CREBBP protein, human; D051548:Histone Acetyltransferases; D050880:p300-CBP Transcription Factors; D006655:Histone Deacetylases; D005947:Glucose
keywords: diabetes; gallic acid; proinflammatory cytokine; · epigenetics