Sulforaphane decreases kidney injury after transplantation in rats: role of mitochondrial damage

Čekauskas, A.; Bruns, Helge; Manikas, Martynas; Herr, Ingrid; Groß, Marie-Luise; Zorn, Markus; Jankevičius, Feliksas; Strupas, Kęstutis; Schemmer, Peter

doi:10.12659/aot.884013

Cited by 20 publications

(10 citation statements)

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“…Thus, the renoprotective effect of SFN can be attributed to the direct removal of excess ROS. Consistently with our findings, the antioxidant effects of SFN have also been reported in previous studies [ 28 , 29 ]. Moreover, SFN also increased the viability of Ioversol-injured HK2 cells.…”

Section: Discussionsupporting

confidence: 94%

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

Zhao

Liao

Zhou

et al. 2016

Oxidative Medicine and Cellular Longevity

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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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Section: Discussionsupporting

confidence: 94%

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

Zhao

Liao

Zhou

et al. 2016

Oxidative Medicine and Cellular Longevity

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“…We examined 5 random biopsies by electron microscopy. We found varying degrees of mitochondrial and proximal tubular injury consistent with patterns observed in ischemia-reperfusion injury (Figure 3) [11,25]. The most notable findings included mitochondrial swelling, apical membrane blebbing, and necrotic luminal debris.…”

Section: Resultssupporting

confidence: 79%

Renal PGC1α May Be Associated with Recovery after Delayed Graft Function

Drury

Zsengellér

Stillman

et al. 2017

Nephron

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Background: Delayed renal graft function (DGF) contributes to the determination of length of hospitalization, risk of acute rejection, and graft loss. Existing tools aid the diagnosis of specific DGF etiologies such as antibody-mediated rejection, but markers of recovery have been elusive. The peroxisome proliferator gamma co-activator-1-alpha (PGC1α) is highly expressed in the renal tubule, regulates mitochondrial biogenesis, and promotes recovery from experimental acute kidney injury. Objectives: We aimed to determine the association between renal allograft PGC1α expression and recovery from delayed graft function. Methods: We retrospectively analyzed patients undergoing renal transplantation at a single center from January 1, 2008 to June 30, 2014. PGC1α expression was assessed by immunostaining and ultrastructural characteristics by transmission electron microscopy. Of 34 patients who underwent renal biopsy for DGF within 30 days of transplant, 21 were included for analysis. Results: Low PGC1α expression was associated with a significantly longer time on dialysis after transplant (median of 35.5 vs. 16 days, p < 0.05) and a significantly higher serum creatinine (sCr) at 4 weeks after transplantation among those who discontinued dialysis (5 vs. 1.65 mg/dL, p < 0.0001). Low PGC1α expression was not associated with higher sCr at 12 weeks after transplantation. Ultrastructural characteristics including apical membrane blebbing and necrotic luminal debris were not informative regarding clinical outcomes. Conclusions: These data suggest that higher PGC1α expression is associated with faster and more complete recovery from DGF. Mitochondrial biogenesis may be a therapeutic target for DGF. Larger studies are needed to validate these findings.

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“…While, SFN has been successfully tested in humans [45], there is no clinical data available in the field of human transplant. However, there are two reports demonstrating protective effects on renal and cardiac grafts [31,32]. Hence, the present findings are promising in that SFN provides a working point for ameliorating intestinal IRI through modulation of leukocyte and platelet activation.…”

Section: Discussionmentioning

confidence: 57%

“…In addition, tissue protection was previously demonstrated by reduced neutrophil infiltration and amended inflammation [31]. Thus, a positive anti-oxidative and anti-inflammatory property was verified in models of brain, heart, kidney and liver IRI [16,28,[30][31][32]. The study presented herein is the first study focusing on anti-inflammatory effects of SFN concentrating on inflammatory in vivo cell trafficking utilizing a murine model of intestinal IRI.…”

Section: Discussionmentioning

confidence: 63%

Sulforaphane Elicits Protective Effects in Intestinal Ischemia Reperfusion Injury

Chen

Mohr

Heitplatz

et al. 2020

IJMS

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Intestinal ischemia reperfusion injury (IRI) is an inherent, unavoidable event of intestinal transplantation, contributing to allograft failure and rejection. The inflammatory state elicited by intestinal IRI is characterized by heightened leukocyte recruitment to the gut, which is amplified by a cross-talk with platelets at the endothelial border. Sulforaphane (SFN), a naturally occurring isothiocyanate, exhibits anti-inflammatory characteristics and has been shown to reduce platelet activation and block leukocyte adhesion. Thus, the aim of this study was to investigate protective effects and mechanism of action of SFN in a murine model of intestinal IRI. Intestinal IRI was induced by superior mesenteric artery occlusion for 30 min, followed by reperfusion for 2 h, 8 h or 24 h. To investigate cellular interactions, leukocytes were in vivo stained with rhodamine and platelets were harvested from donor animals and ex vivo stained. Mice (C57BL/6J) were divided into three groups: (1) control, (2) SFN treatment 24 h prior to reperfusion and (3) SFN treatment 24 h prior to platelet donation. Leukocyte and platelet recruitment was analyzed via intravital microscopy. Tissue was analyzed for morphological alterations in intestinal mucosa, barrier permeability, and leukocyte infiltration. Leukocyte rolling and adhesion was significantly reduced 2 h and 8 h after reperfusion. Mice receiving SFN treated platelets exhibited significantly decreased leukocyte and platelet recruitment. SFN showed protection for intestinal tissue with less damage observed in histopathological and ultrastructural evaluation. In summary, the data presented provide evidence for SFN as a potential therapeutic strategy against intestinal IRI.

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Sulforaphane decreases kidney injury after transplantation in rats: role of mitochondrial damage

Abstract: SFN ameliorates ischemia/reperfusion injury after KTx, most likely through anti-oxidative effects.

Cited by 20 publications

References 0 publications

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

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

Renal PGC1α May Be Associated with Recovery after Delayed Graft Function

Sulforaphane Elicits Protective Effects in Intestinal Ischemia Reperfusion Injury

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