Open Access Journal Indian Journal of Medical Research and Pharmaceutical Sciences February 2016; 3(2) ISSN: ISSN: 2349-5340 Impact Factor (PIF): 2.672 © Indian Journal of Medical Research and Pharmaceutical Sciences http://www.ijmprs.com/ [80] BOLDINE TREATMENT PREVENTS KIDNEY DAMAGE IN RATS WITH 5/6 NEPHRECTOMY 1,2 Gonzalo I. Gómez, Victoria Velarde* Departamento de Fisiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Alameda #340, Santiago, Chile. Keywords: Chronic Renal Failure, Antioxidant, Oxidative Stress, Fibrosis, (S)-2,9-Dihydroxy-1,10- dimethoxy-aporphine Abstract Chronic renal failure(CRF) results in the progressive loss of kidney function toward a terminal stage. It is manifested by the advancing decrease in glomerular filtration, due to morphological alterations such as tubular necrosis and glomerular sclerosis. Moreover, oxidative stress increases in patients with CRF. Therefore, the use of natural products, such as the antioxidant boldine, has been observed to be a promising focus of research. We propose that boldine treatment prevents kidney damage in 5/6 nephrectomized(5/6NX) rats. Rats(n=5/group) were treated with boldine(50mg/kg/day, gavage) for 28 days after 5/6NX; kidney function was evaluated measuring urinary protein/creatinine ratio(Uprot/Ucrea); and oxidative stress measuring thiobarbituric acid reactive substances(TBARS). ED-1(marker of inflammation), Col III(marker of kidney damage) and Vimentin(recovery marker) were evaluated by Western blot and immunohistochemistry. Uprot/Ucrea ratio(4.53±1.29AU in 5/6NX+Boldine; 13.30±4.14AU in 5/6NX) and TBARS(39.52±3.73nmol/g in 5/6NX+Boldine; 62.42±1.05nmol/g in 5/6NX) were lower in 5/6NX+boldine rats than in 5/6NX rats p<0.05. In 5/6NX +boldine rats, levels of ED-1 and Col III were lower compared to 5/6NX rats. Vimentin(mesenchymal marker) was increased in 5/6NX+boldine rats, compared with 5/6NX rats. These results suggest that boldine protects the kidney in rats with 5/6NX and that boldine could potentially be used as a nutraceutic. Introduction Chronic renal failure (CRF) is a condition that results in the progressive loss of kidney function until reaching a terminal stage (1). It is manifested by an advancing decrease in glomerular filtration rate (GFR), resulting from a rise in damaged nephrons, in addition to tubular homeostasis and, finally, failure of the organ’s hormonal functions (1-2). Unlike acute renal failure (ARF), where an abrupt but reversible decline in renal function is observed (3), CRF involves the progressive recruitment of nephrons, which could have varying degrees of structural and functional damage (4). CRF has different etiologies. Independent of the cause, however, the morphological characteristics, such as tubular necrosis and glomerular sclerosis, are similar (5). The prevalence of this condition has increased worldwide and it has been estimated that over 10% of adults in developed countries suffer from some degree of CRF. For this reason, the search for a treatment for this disease is a major research topic in nephrology (6). CRF is characterized by atrophy and/or tubular dilation, interstitial leukocyte infiltration and increased deposition of the extracellular matrix, eventually developing into renal interstitial fibrosis (7). Macrophage infiltration occurs at several sites of the inflamed kidney, and their presence in the interstitium and the glomerulus contributes to tissue