Sulforaphane Attenuates Contrast‐Induced Nephropathy in Rats via Nrf2/HO‐1 Pathway

Abstract

Background. Oxidative stress plays an important role in the pathogenesis of contrast-induced nephropathy (CIN). The aim of this study was to investigate the antioxidant effects of sulforaphane (SFN) in a rat model of CIN and a cell model of oxidative stress in HK2 cells. Methods. Rats were randomized into four groups (n = 6 per group): control group, Ioversol group (Ioversol-induced CIN), Ioversol + SFN group (CIN rats pretreated with SFN), and SFN group (rats treated with SFN). Renal function tests, malondialdehyde (MDA), and reactive oxygen species (ROS) were measured. Western blot, real-time polymerase chain reaction analysis, and immunohistochemical analysis were performed for nuclear factor erythroid-derived 2-like 2 (Nrf2) and heme oxygenase-1 (HO-1) detection. Results. Serum blood urea nitrogen (BUN), creatinine, and renal tissue MDA were increased after contrast exposure. Serum BUN, creatinine, and renal tissue MDA were decreased in the Ioversol + SFN group as compared with those in the Ioversol group. SFN increased the expression of Nrf2 and HO-1 in CIN rats and in Ioversol-induced injury HK2 cells. SFN increased cell viability and attenuated ROS level in vitro. Conclusions. SFN attenuates experimental CIN in vitro and in vivo. This effect is suggested to activate the Nrf2 antioxidant defenses pathway.

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tert-Butylhydroquinone Treatment Alleviates Contrast-Induced Nephropathy in Rats by Activating the Nrf2/Sirt3/SOD2 Signaling Pathway

“…Nrf2 is an important transcription factor belonging to the E26 transformation-specific (ETS) factor family that regulates the cellular resistance to oxidants, including radiocontrast agents [26]. Previous studies have shown that Nrf2 plays a renoprotective role in CIN [25,27]. Sirt3, which is an NAD + -dependent deacetylase localized in the mitochondrial matrix, regulates a variety of cellular processes, including oxidative stress, ATP generation, and energy metabolism.…”

The Association Between Oxidative Stress Alleviation via Sulforaphane-Induced Nrf2-HO-1/NQO-1 Signaling Pathway Activation and Chronic Renal Allograft Dysfunction Improvement

“…Continuous SFN intervention for 3 months also prevented the diabetic induction of renal dysfunction, fibrosis, inflammation and oxidative damage by activating the Nrf2 and its downstream antioxidant proteins in a type 1 diabetic mouse model [17]. In addition, it was validated in a rat model that SFN-induced activation of the Nrf2 signaling pathway ameliorated unilateral ureteral obstruction-induced renal damage and alleviated renal dysfunction and pathological changes caused by contrast-induced nephropathy [18, 19]. Furthermore, animals with deficient or dysfunctional Nrf2 signaling pathway are more susceptible to various kidney diseases, including acute kidney injury, lupus-like autoimmune nephritis, hyperglycemia-induced renal injury and progressive focal glomerulosclerosis [20-23].…”