Antioxidant and renoprotective effects of paricalcitol on experimental contrast-induced nephropathy model

E Ari, A E Kedrah, Y Alahdab, G Bulut, Z Eren, O Baytekin, D Odabasi, E Ari, A E Kedrah, Y Alahdab, G Bulut, Z Eren, O Baytekin, D Odabasi

Abstract

Objectives: The aim of the study was to assess the effect of paricalcitol on the experimental contrast-induced nephropathy (CIN) model. We hypothesised that paricalcitol may prevent CIN.

Methods: 32 Wistar albino rats were divided into four groups (n=8 each): control group, paricalcitol group, CIN group and paricalcitol plus CIN group. Paricalcitol (0.4 µg kg(-1) day(-1)) was given intraperitoneally for 5 consecutive days prior to induction of CIN. CIN was induced at day 4 by intravenous injection of indometacin (10 mg kg(-1)), Nω-nitro-L-arginine methyl ester (L-NAME, 10 mg kg(-1)) and meglumine amidotrizoate (6 ml kg(-1)). Renal function parameters, oxidative stress biomarkers, histopathological findings and vascular endothelial growth factor (VEGF) immunoexpression were evaluated.

Results: The paricalcitol plus CIN group had lower mean serum creatinine levels (p=0.034) as well as higher creatinine clearance (p=0.042) than the CIN group. Serum malondialdehyde and kidney thiobarbituric acid-reacting substances levels were significantly lower in the paricalcitol plus CIN group than in the CIN group (p=0.024 and p=0.042, respectively). The mean scores of tubular necrosis (p=0.024), proteinaceous casts (p=0.038), medullary congestion (p=0.035) and VEGF immunoexpression (p=0.018) in the paricalcitol plus CIN group were also significantly lower.

Conclusion: This study demonstrates the protective effect of paricalcitol in the prevention of CIN in an experimental model.

Figures

Figure 1
Figure 1
Histopathological findings of the study groups (haematoxylin and eosin staining, original magnification, ×200). Normal histology in (a) control and (b) paricalcitol groups. (c) Tubular necrosis areas in renal outer medulla of contrast-induced nephropathy (CIN) group. (d) Healthy tubular cells in renal outer medulla of paricalcitol plus CIN group.
Figure 2
Figure 2
Immunoexpression of vascular endothelial growth factor (VEGF) in the study groups (original magnification, ×200). No immunoexpression of VEGF of tubular cells in the outer medulla of (a) the control, (b) paricalcitol and (d) paricalcitol + contrast-induced nephropathy (CIN) groups. (c) Severe immunoexpression of VEGF of tubular cells in the outer medulla of the CIN group.

Source: PubMed

3
Prenumerera