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Monoaminoguanidine prevents sorbitol accumulation, nonenzymatic protein glycosylation and development of kidney lesions in diabetic rats.

作者信息

Kumari K, Murthy P S, Sahib M K

机构信息

Division of Biochemistry and Toxicology, Central Drug Research Institute, Lucknow, India.

出版信息

Experientia. 1991 Mar 15;47(3):252-4. doi: 10.1007/BF01958151.

DOI:10.1007/BF01958151
PMID:2009934
Abstract

Monoaminoguanidine administration (25 mg/kg b.wt, i.p. for 14 weeks) to alloxan diabetic rats (blood glucose greater than or equal to 250 mg/dl) decreased the nonenzymatic protein glycosylation and sorbitol levels. It prevented development of Armanni-Ebstein tubular lesions, pathological changes in the glomerular capillary tufts and glomerular basement membrane thickening in the kidney.

摘要

相似文献

1
Monoaminoguanidine prevents sorbitol accumulation, nonenzymatic protein glycosylation and development of kidney lesions in diabetic rats.
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2
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本文引用的文献

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Protein measurement with the Folin phenol reagent.使用福林酚试剂进行蛋白质测定。
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6
Nonenzymatic glycosylation: role in the pathogenesis of diabetic complications.非酶糖基化：在糖尿病并发症发病机制中的作用
Clin Chem. 1986 Oct;32(10 Suppl):B37-41.
7
Aminoguanidine prevents diabetes-induced arterial wall protein cross-linking.氨基胍可防止糖尿病引起的动脉壁蛋白交联。
Science. 1986 Jun 27;232(4758):1629-32. doi: 10.1126/science.3487117.
8
The involvement of aldose reductase in diabetic complications.
Diabetes Metab Rev. 1988 Jun;4(4):323-37. doi: 10.1002/dmr.5610040403.
9
Evidence for existence of polyol pathway in cultured rat mesangial cells.培养的大鼠系膜细胞中多元醇途径存在的证据。
Diabetes. 1987 Feb;36(2):240-3. doi: 10.2337/diab.36.2.240.