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Titolo:
Only limited effects of aminoguanidine treatment on peripheral nerve function, (Na+,K+)-ATPase activity and thrombomodulin expression in streptozotocin-induced diabetic rats
Autore:
Wada, R; Sugo, M; Nakano, M; Yagihashi, S;
Indirizzi:
Hirosaki Univ, Sch Med, Dept Pathol, Hirosaki, Aomori 0368562, Japan Hirosaki Univ Hirosaki Aomori Japan 0368562 rosaki, Aomori 0368562, Japan Mitsubishi Gas Chem Co Inc, Niigata, Japan Mitsubishi Gas Chem Co Inc Niigata Japan as Chem Co Inc, Niigata, Japan
Titolo Testata:
DIABETOLOGIA
fascicolo: 6, volume: 42, anno: 1999,
pagine: 743 - 747
SICI:
0012-186X(199906)42:6<743:OLEOAT>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
PLASMA THROMBOMODULIN; NITRIC-OXIDE; NONENZYMATIC GLYCATION; FREE-RADICALS; IDENTIFICATION; TRIPHOSPHATASE; GLYCOSYLATION; COMPLICATIONS; ENDOTHELIUM; INHIBITION;
Keywords:
experimental diabetic neuropathy; aminoguanidine; insulin; nerve conduction velocity; (Na+,K+)-ATPase activity; thrombomodulinIntroduction;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Yagihashi, S Hirosaki Univ, Sch Med, Dept Pathol, 5 Zaifu Cho, Hirosaki, Aomori 0368562, Hirosaki Univ 5 Zaifu Cho Hirosaki Aomori Japan 0368562 8562,
Citazione:
R. Wada et al., "Only limited effects of aminoguanidine treatment on peripheral nerve function, (Na+,K+)-ATPase activity and thrombomodulin expression in streptozotocin-induced diabetic rats", DIABETOLOG, 42(6), 1999, pp. 743-747

Abstract

Aims/hypothesis. Aminoguanidine, a potent anti-glycation reagent, is knownto be beneficial in experimental diabetic neuropathy. In this study, we explored the mechanisms of how aminoguanidine inhibits neuropathic changes indiabetes and compared its effects with those of insulin treatment. Methods. Wistar rats, aged 8 weeks, were made diabetic by streptozotocin and given aminoguanidine dissolved in drinking water (1 g/l) for 8 weeks. Effects of daily insulin (protamine-zinc) treatment were also examined for comparison. At the end of the 8 weeks, we examined the peripheral nerve function and (Na+,K+)-ATPase activity and their relation to serum thrombomodulinconcentrations that are considered as a marker of endothelial injury. Results. Aminoguanidine treatment reduced the diabetes-induced decrease intibial nerve conduction velocity by 47 % (p < 0.05 vs untreated diabetic rats) and inhibited the loss of sciatic nerve (Na+,K+)-ATPase activity by 54% (p < 0.05 VS untreated diabetic rats). Insulin-treatment of diabetic rats restored these variables by 83% and 75%, respectively (both, p < 0.01 vs untreated diabetic rats). Thrombomodulin concentrations were increased (p <0.01) in diabetic rats compared with those in non-diabetic controls and unaffected by aminoguanidine treatment. In contrast, the concentrations remained within the normal range in the insulin-treated group. Conclusion/interpretation. Although aminoguanidine treatment improved nerve conduction velocity and (Na+,K+)-ATPase activity, its effects were considerably less than those of insulin and were not apparent in some measures ofendothelial cell injury.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/09/20 alle ore 02:14:06