Effect of lignin-derived lignophenols on vascular oxidative stress and inflammation in streptozotocin-induced diabetic rats.
Lignophenols (LP) are the derivatives of native lignin, which is an abundant organic polymer in the plant kingdom. This study investigated whether LP can attenuate vascular oxidative stress and inflammation in streptozotocin (STZ)-induced diabetic rats. The diabetic rats induced by a single intravenous injection of STZ were randomly divided into two groups fed either 0 or 1.0% LP-containing diet. After 5 weeks of treatment, the superoxide (O(2)(-)) production, mRNA expression levels of nicotinamide adenine dinucleotide (phosphate) (NAD(P)H) oxidase subunits, monocyte chemoattractant protein-1 (MCP-1) and its receptor C-C chemokine receptor 2 (CCR2), and protein expression level of inducible nitric oxide synthase (iNOS) were examined in the aorta of vehicle-injected control and diabetic rats treated with or without LP. The increased O(2)(-) production and mRNA expression levels of NAD(P)H oxidase subunits Nox4 and p47phox were found to be significantly reduced in the aorta of diabetic rats treated with LP. The mRNA expression of MCP-1 and CCR2, and the protein expression of iNOS were found to be increased in the aorta of untreated diabetic rats, whereas these levels were significantly lower in the LP-treated group. These findings suggest that LP could attenuate vascular oxidative stress and/or inflammation via inhibition of NAD(P)H oxidase. This may lead to an improvement in the vascular impairment of diabetes.
Department of Nutrition, Faculty of Health Sciences, Aomori University of Health and Welfare, Hamadate, Aomori, Japan.
Yuuka
Y
Mukai
Toshio
T
Norikura
Shuzo
S
Fujita
Keigo
K
Mikame
Masamitsu
M
Funaoka
Shin
S
Sato
D000080242:8-Hydroxy-2'-Deoxyguanosine; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D000975:Antioxidants / Q000494:pharmacology*; D001011:Aorta / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D001786:Blood Glucose / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000652:urine; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D029964:Fagus; D007249:Inflammation / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000517:prevention & control*; D008031:Lignin / Q000494:pharmacology*; D008055:Lipids / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D000074663:NADPH Oxidase 4; D019255:NADPH Oxidases / Q000235:genetics / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D010636:Phenols / Q000494:pharmacology*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D054390:Receptors, CCR2 / Q000235:genetics / Q000378:metabolism; D013481:Superoxides / Q000378:metabolism; D013997:Time Factors
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D001786:Blood Glucose; C491766:Ccl2 protein, rat; C515336:Ccr2 protein, rat; D018932:Chemokine CCL2; D008055:Lipids; D010636:Phenols; D012333:RNA, Messenger; D054390:Receptors, CCR2; D013481:Superoxides; D008315:Malondialdehyde; D000080242:8-Hydroxy-2'-Deoxyguanosine; D008031:Lignin; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D000074663:NADPH Oxidase 4; D019255:NADPH Oxidases; C498911:Nox4 protein, rat; C060505:neutrophil cytosolic factor 1; D003849:Deoxyguanosine