Effects of Vitamin D3 (Cholecalciferol) on Adriamycin-Induced Nephrotoxicity

被引:11
作者
Dabak, Durrin Ozlem [1 ,2 ]
Kuloglu, Tuncay [1 ,2 ]
Ozercan, Mehmet Resat [3 ]
机构
[1] Firat Univ, Sch Med, Dept Histol, TR-23119 Elazig, Turkey
[2] Firat Univ, Sch Med, Dept Embryol, TR-23119 Elazig, Turkey
[3] Firat Univ, Sch Med, Dept Pathol, TR-23119 Elazig, Turkey
关键词
adriamycin; nephrotoxicity; vitamin D; INDUCED NEPHROTIC SYNDROME; INJURY; CELLS; MODEL; MACROPHAGES; PROGRESSION; GLOMERULOSCLEROSIS; NEPHROPATHY; DEPLETION; SEQUENCE;
D O I
10.1080/08860220902883020
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Although immune-mediated pathogenesis in adriamycin (ADR)-induced nephropathy has been proposed recently, studies are lacking about the effects of immunmodulators, such as vitamin D, on ADR-induced nephrotoxicity. We hypothesized that vitamin D-3 (cholecalciferol) would be beneficial on ADR-induced nephropathy because of its immunmodulatory properties. Eighteen male Wistar rats were divided into three groups (n = 6): group 1 (control), group 2 (single ADR injection intravenously), and group 3 (similar single ADR injection intravenously + daily oral cholecalciferol for 21 days) were used in the study. A single high dose of ADR resulted in increased urinary protein: creatinine ratio for all three weeks of the experiment in both groups 2 and 3 compared with the controls. Histological examination of the kidney tissue revealed distinct tubular lesions as tubular necrosis, hyaline casts in tubular lumen, tubular degeneration, tubular dilatation, and tubular vacuolization in group 2 compared with group 1. These tubular lesions were significantly reduced in group 3 compared to group 2. The results of this study indicate that cholecalciferol causes satisfactory tubulointerstitial recovery in ADR-induced nephrotoxicity in rats.
引用
收藏
页码:400 / 405
页数:6
相关论文
共 29 条
[1]   Antiproteinuric effect of oral paricalcitol in chronic kidney disease [J].
Agarwal, R ;
Acharya, M ;
Tian, J ;
Hippensteel, RL ;
Melnick, JZ ;
Qiu, P ;
Williams, L ;
Batlle, D .
KIDNEY INTERNATIONAL, 2005, 68 (06) :2823-2828
[2]  
BERTANI T, 1982, LAB INVEST, V46, P16
[3]   L-carnitine ameliorates doxorubicin-induced nephrotic syndrome in rats [J].
Boonsanit, Dolrudee ;
Kanchanapangka, Sumolaya ;
Buranakarl, Chollada .
NEPHROLOGY, 2006, 11 (04) :313-320
[4]   The cytoprotective role of a low-molecular-weight heparin fragment studied in an experimental model of glomerulotoxicity [J].
Deepa, PR ;
Varalakshmi, P .
EUROPEAN JOURNAL OF PHARMACOLOGY, 2003, 478 (2-3) :199-205
[5]   Altered antioxidant defence in a mouse adriamycin model of glomerulosclerosis [J].
Deman, A ;
Ceyssens, B ;
Pauwels, M ;
Zhang, JG ;
Vanden Houte, K ;
Verbeelen, D ;
Van den Branden, C .
NEPHROLOGY DIALYSIS TRANSPLANTATION, 2001, 16 (01) :147-150
[6]   Vitamin D [J].
Dusso, AS ;
Brown, AJ ;
Slatopolsky, E .
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 2005, 289 (01) :F8-F28
[7]  
Guyton AC, 2000, TXB MED PHYSL, P904
[8]   22-oxacalcitriol prevents progressive glomerulosclerosis without adversely affecting calcium and phosphorus metabolism in subtotally nephrectomized rats [J].
Hirata, M ;
Makibayashi, K ;
Katsumata, K ;
Kusano, K ;
Watanabe, T ;
Fukushima, N ;
Doi, T .
NEPHROLOGY DIALYSIS TRANSPLANTATION, 2002, 17 (12) :2132-2137
[9]   Prevalence of calcidiol deficiency in CKD: A cross-sectional study across latitudes in the united states [J].
LaClair, RE ;
Hellman, RN ;
Karp, SL ;
Kraus, M ;
Ofner, S ;
Li, Q ;
Graves, KL ;
Moe, SM .
AMERICAN JOURNAL OF KIDNEY DISEASES, 2005, 45 (06) :1026-1033
[10]   CD4+CD25+ regulatory T cells protect against injury in an innate murine model of chronic kidney disease [J].
Mahajan, Deepika ;
Wang, Yiping ;
Qin, Xiahong ;
Wang, Ying ;
Zheng, Guoping ;
Wang, Yuan Min ;
Alexander, Stephen I. ;
Harris, David C. H. .
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2006, 17 (10) :2731-2741