Ferulic acid prevents methylglyoxal-induced protein glycation, DNA damage, and apoptosis in pancreatic β-cells.
Methylglyoxal (MG) can react with amino acids of proteins to induce protein glycation and consequently the formation of advanced glycation end-products (AGEs). Previous studies reported that ferulic acid (FA) prevented glucose-, fructose-, and ribose-induced protein glycation. In this study, FA (0.1-1 mM) inhibited MG-induced protein glycation and oxidative protein damage in bovine serum albumin (BSA). Furthermore, FA (0.0125-0.2 mM) protected against lysine/MG-mediated oxidative DNA damage, thereby inhibiting superoxide anion and hydroxyl radical generation during lysine and MG reaction. In addition, FA did not have the ability to trap MG. Finally, FA (0.1 mM) pretreatment attenuated MG-induced decrease in cell viability and prevented MG-induced cell apoptosis in pancreatic β-cells. The results suggest that FA is capable of protecting β-cells from MG-induced cell damage during diabetes.
Department of Clinical Chemistry, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, 10330, Thailand.|Research Group of Herbal Medicine for Prevention and Therapeutic of Metabolic Diseases, Chulalongkorn University, Bangkok, 10330, Thailand.
Weerachat
W
Sompong
Department of Comparative Biomedical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA, 70803, USA.
Henrique
H
Cheng
Research Group of Herbal Medicine for Prevention and Therapeutic of Metabolic Diseases, Chulalongkorn University, Bangkok, 10330, Thailand. sirichai.a@chula.ac.th.|Department of Nutrition and Dietetics, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, 10330, Thailand. sirichai.a@chula.ac.th.
Sirichai
S
Adisakwattana
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D015415:Biomarkers / Q000378:metabolism; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D003373:Coumaric Acids / Q000494:pharmacology*; D053960:DNA Breaks / Q000187:drug effects; D004249:DNA Damage / Q000187:drug effects*; D016166:Free Radical Scavengers / Q000494:pharmacology*; D017127:Glycation End Products, Advanced / Q000037:antagonists & inhibitors / Q000378:metabolism; D006031:Glycosylation / Q000187:drug effects; D050417:Insulin-Secreting Cells / Q000187:drug effects* / Q000378:metabolism; D009994:Osmolar Concentration; D016877:Oxidants / Q000037:antagonists & inhibitors / Q000633:toxicity; D018384:Oxidative Stress / Q000187:drug effects; D050050:Protein Carbonylation / Q000187:drug effects; D011499:Protein Processing, Post-Translational / Q000187:drug effects*; D011765:Pyruvaldehyde / Q000037:antagonists & inhibitors / Q000633:toxicity; D051381:Rats; D012710:Serum Albumin, Bovine / Q000037:antagonists & inhibitors / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000737:chemistry / Q000378:metabolism
D015415:Biomarkers; D003373:Coumaric Acids; D016166:Free Radical Scavengers; D017127:Glycation End Products, Advanced; D016877:Oxidants; D017392:Thiobarbituric Acid Reactive Substances; C081628:advanced glycation end products-bovine serum albumin; D012710:Serum Albumin, Bovine; D011765:Pyruvaldehyde; C004999:ferulic acid
Apoptosis; Ferulic acid; Methylglyoxal; Oxidative DNA damage; Pancreatic β-cell; Protein glycation