Role of maltol in advanced glycation end products and free radicals: in-vitro and in-vivo studies.
Inhibitors of advanced glycation end products (AGEs) have potential as preventive agents against diabetic complications. In-vitro AGE inhibitory activity, transition metal chelating, and free radical scavenging activity tests have been used to screen for and identify effective AGE inhibitors. In an ongoing project to elucidate AGE inhibiting active components of heat-processed ginseng, maltol was selected for more detailed investigation. Although there are several lines of evidence concerning the antioxidant activity of maltol, the in-vitro and in-vivo inhibitory effects of maltol on AGE generation have not been evaluated. In the present study, the in-vitro AGE inhibitory effects and free radical scavenging activity of maltol were investigated. In addition, the in-vivo therapeutic potential of maltol against diabetic renal damage was tested using streptozotocin (STZ)-diabetic rats. Maltol showed a stronger AGE inhibitory effect than aminoguanidine, a well known AGE inhibitor. In addition, the hydroxyl radical scavenging activity of maltol on electron spin resonance (ESR) spectrometry was slightly stronger than that of aminoguanidine. Therefore, maltol was found to have stronger in-vitro AGE inhibiting activity compared with aminoguanidine. The administration of 50 mgkg(-1) per day of maltol suppressed the elevated serum levels of glycosylated protein, renal fluorescent AGEs, carboxymethyllysine, receptors for AGEs, and nuclear factor-kappaB p65 in diabetic control rats. These beneficial effects of maltol against STZ-diabetic renal damage were thought to result from its free radical scavenging and AGE inhibitory effects.
Kang
Ki Sung
KS
Institute of Natural Medicine, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.
Yamabe
Noriko
N
Kim
Hyun Young
HY
Yokozawa
Takako
T
D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D003404:Creatinine / Q000097:blood; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000150:complications / Q000188:drug therapy; D003928:Diabetic Nephropathies / Q000209:etiology / Q000517:prevention & control; D004578:Electron Spin Resonance Spectroscopy; D016166:Free Radical Scavengers / Q000008:administration & dosage / Q000737:chemistry / Q000494:pharmacology*; D005609:Free Radicals / Q000737:chemistry; D017127:Glycation End Products, Advanced / Q000037:antagonists & inhibitors / Q000737:chemistry / Q000378:metabolism*; D006146:Guanidines / Q000008:administration & dosage / Q000737:chemistry / Q000494:pharmacology; D008239:Lysine / Q000031:analogs & derivatives / Q000187:drug effects / Q000378:metabolism; D008297:Male; D011507:Proteinuria / Q000209:etiology / Q000517:prevention & control; D011753:Pyrones / Q000008:administration & dosage / Q000737:chemistry / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000378:metabolism; D012709:Serum Albumin / Q000187:drug effects / Q000378:metabolism; D013311:Streptozocin; D051996:Transcription Factor RelA / Q000187:drug effects / Q000378:metabolism; D000093423:Glycated Serum Albumin
D001786:Blood Glucose; D016166:Free Radical Scavengers; D005609:Free Radicals; D017127:Glycation End Products, Advanced; D006146:Guanidines; D011753:Pyrones; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic; D012709:Serum Albumin; D051996:Transcription Factor RelA; C008316:maltol; D013311:Streptozocin; C048496:N(6)-carboxymethyllysine; D003404:Creatinine; D008239:Lysine; C004479:pimagedine; D000093423:Glycated Serum Albumin