N-hexacosanol ameliorates streptozotocin-induced diabetic rat nephropathy

• Published in: European journal of pharmacology 2006-08, Vol.544 (1), p.132-137
• Main Authors: Saito, Motoaki, Kinoshita, Yukako, Satoh, Itaru, Shinbori, Chiko, Kono, Tomoharu, Hanada, Takuya, Uemasu, Jiro, Suzuki, Hiroto, Yamada, Masashi, Satoh, Keisuke
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Blood Urea Nitrogen; Creatinine - metabolism; Diabetes; Diabetes. Impaired glucose tolerance; Diabetic Nephropathies - chemically induced; Diabetic Nephropathies - pathology; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Fatty Alcohols - pharmacology; Insulin - metabolism; Kidneys; Male; Malonaldehyde; Malondialdehyde - metabolism; Medical sciences; N-hexacosanol; Nephrology. Urinary tract diseases; Nephropathy; Pharmacology. Drug treatments; PKC (protein kinase C); Protein Kinase C - metabolism; Rats; Rats, Sprague-Dawley; Streptozocin - pharmacology; TGF-β 1 (transforming growth factor beta-1); Transforming Growth Factor beta1 - metabolism; Urinary system involvement in other diseases. Miscellaneous
• ISSN: 0014-2999; 1879-0712
• DOI: 10.1016/j.ejphar.2006.06.001

In this study we investigated the effects of N-hexacosanol on streptozotocin-induced rat diabetic nephropathy. Diabetes was induced in 8-week-old male Sprague–Dawley rats by administering an intraperitoneal injection of streptozotocin (50 mg/kg). The rats were divided into four groups and maintained for 8 weeks: control rats, diabetic rats without treatment with N-hexacosanol, and diabetic rats treated with N-hexacosanol (2 mg/kg and 8 mg/kg i.p. every day). Although N-hexacosanol failed to modify the diabetic status, increases in serum creatinine as well as in kidney weight were significantly reduced. The malonaldehyde and transforming growth factor beta-1 (TGF-β 1) concentrations as well as the protein kinase C (PKC) activities in the diabetic kidney were significantly higher than those of the control, which were decreased by treatment with N-hexacosanol. Histological examinations revealed that N-hexacosanol significantly ameliorated diabetic-induced tubulointerstitial pathological changes. Our data suggest that N-hexacosanol could prevent increases in the malonaldehyde and TGF-β 1 concentrations and PKC activities in the kidney, and ameliorate diabetic-induced nephropathy.