Astaxanthin attenuates contrast-induced acute kidney injury in rats via ROS/NLRP3 inflammasome.

Abstract

To explore the protective effect and mechanism of astaxanthin on the kidney of rats with contrast-induced acute kidney injury. Forty SD rats were randomly divided into five groups: Control group (CON); Astaxanthin control group (AST); Contrast media group (CM); Astaxanthin pre-treatment group (AST + CM); N-acetylcysteine pre-treatment group (NAC + CM), each group with eight rats. The rats were killed 72h after the modeling, the blood supernatant and kidneys were collected, and then the serum creatinine and blood urea nitrogen levels were measured; HE staining was used to observe the pathological changes in kidney tissue; TUNEL was used to detect apoptosis level in renal tubular epithelial cells; frozen section was used to observe the expression of ROS in renal tissue by reactive oxygen staining; the expression of NLRP3, ASC, caspase-1, IL-1β, IL-18 were detected by immunohistochemistry and western blot. The CI-AKI rat model was induced by iohexol. Then the elevated level of ROS activated the inflammatory response mediated by NLRP3 inflammasome (NLRP3, ASC, caspase-1). Subsequently, the increase in renal tubular epithelial cell apoptosis caused the destruction of the pathological structure of the kidney and finally led to renal impairment. While after the pretreatment of astaxanthin, the level of ROS was decreased. The activation level of NLRP3 inflammasome and its mediated inflammatory response were alleviated significantly. Eventually, the level of renal tubular epithelial cell apoptosis and renal damage were significantly mitigated. Astaxanthin can protect the kidney in CI-AKI by inhibiting the activation of NLRP3 inflammasome-IL-1β/IL-18 through inhibition of the production of ROS.