Nephroprotective effect of Astaxanthin in cisplatin-induced renal injury in a rat model

COŞKUN et al.: PROTECTIVE ROLE OF ASTAXANTHIN ON CISPLATIN-INDUCED NEPHROTOXICITY IN RATS

Abstract

This study investigates the possible protective effects of astaxanthin (AX) against cisplatin (CP)-induced nephrotoxicity. The nephroprotective effect of AX against cisplatin-induced inflammation-induced renal injury was evaluated by biochemical and histopathologic analysis. Five groups were examined: saline control, DMSO carrier, AX (50 mg/kg/day, i.p., 7 days), CP (10 mg/kg, i.p.), and AX+ CP. Renal function (serum creatinine, BUN, and urinary KIM-1) and markers of inflammation (IL-1β, IL-6, TNF-α, NF-κB, and COX-2) were evaluated in kidney tissues using ELISA. Histopathologic changes were assessed using hematoxylin and eosin staining. It was determined that single-dose CP administration to rats increased BUN, Cr, and Kim-1 values and caused histopathologic renal toxicity in this group. AX treatment significantly reversed the acute renal injury caused by CP. A statistically significant increase in TNF-α, IL-6, IL-1β, COX-2, and NF-κB concentration levels was observed in the CP group (p<0.05). In contrast, a statistically significant decrease was observed in the AX-treated group (p<0.05). Notably, COX-2 and NF-κB levels were significantly elevated in the CP-treated group, while AX treatment effectively down-regulated these inflammatory markers. In addition, histopathologic examination revealed focal mononuclear cell infiltration areas in the CP-induced interstitial region, congestion areas in the interstitial region, degenerative changes and focal necrosis areas in tubular epithelial cells, enlargement of the bowman space, and hyperemia. Histopathologic examination showed that AX attenuated renal injury. The findings of the present study suggest that AX may provide new opportunities to understand its anti-inflammatory properties better and that the significant reduction of inflammatory cytokine levels in kidney tissue by AX may be related to its anti-inflammatory effect, thus suggesting that it may be a candidate therapeutic molecule against CP-induced nephrotoxicity. We recommend that the ability of AX to limit the increase of inflammatory mediators in kidney tissue may be promising for further clinical applications in protecting against CP-induced kidney injury or at least reducing its adverse effects.