Sulforaphane Elicits Protective Effects in Intestinal Ischemia Reperfusion Injury

Chen, Zhiquan; Mohr, Annika; Heitplatz, Barbara; Hansen, Uwe; Pascher, Andreas; Brockmann, Jens; Becker, Felix

doi:10.3390/ijms21155189

Cited by 7 publications

(5 citation statements)

References 51 publications

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“…It was previously reported that administration of SFN inhibits leukocyte infiltration into tissues [25,30]. This effect may be attributed to the antioxidant and anti-inflammatory properties of SFN, as well as its ability to suppress the expression of vascular endothelial cell adhesion factors, thus suppressing infiltration.…”

Section: Discussionmentioning

confidence: 91%

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Sulforaphane Attenuates Neutrophil ROS Production, MPO Degranulation and Phagocytosis, but Does Not Affect NET Formation Ex Vivo and In Vitro

Wakasugi-Onogi,

Ma,

Ruhee

et al. 2023

IJMS

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Sulforaphane has several effects on the human body, including anti-inflammation, antioxidation, antimicrobial and anti-obesity effects. In this study, we examined the effect of sulforaphane on several neutrophil functions: reactive oxygen species (ROS) production, degranulation, phagocytosis, and neutrophil extracellular trap (NET) formation. We also examined the direct antioxidant effect of sulforaphane. First, we measured neutrophil ROS production induced by zymosan in whole blood in the presence of 0 to 560 µM sulforaphane. Second, we examined the direct antioxidant activity of sulforaphane using a HOCl removal test. In addition, inflammation-related proteins, including an azurophilic granule component, were measured by collecting supernatants following ROS measurements. Finally, neutrophils were isolated from blood, and phagocytosis and NET formation were measured. Sulforaphane reduced neutrophil ROS production in a concentration-dependent manner. The ability of sulforaphane to remove HOCl is stronger than that of ascorbic acid. Sulforaphane at 280 µM significantly reduced the release of myeloperoxidase from azurophilic granules, as well as that of the inflammatory cytokines TNF-α and IL-6. Sulforaphane also suppressed phagocytosis but did not affect NET formation. These results suggest that sulforaphane attenuates neutrophil ROS production, degranulation, and phagocytosis, but does not affect NET formation. Moreover, sulforaphane directly removes ROS, including HOCl.

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Section: Discussionmentioning

confidence: 91%

“…This suggests that Nrf2 may not be involved in phagocytosis. Interestingly, several studies have demonstrated that SFN impacts leukocyte adhesion [30,31]. Based on these observations, it is possible that SFN regulates neutrophil adhesion factors, and thereby inhibits phagocytosis and degranulation by altering adhesion factors.…”

Section: Discussionmentioning

confidence: 99%

Sulforaphane Attenuates Neutrophil ROS Production, MPO Degranulation and Phagocytosis, but Does Not Affect NET Formation Ex Vivo and In Vitro

Wakasugi-Onogi,

Ma,

Ruhee

et al. 2023

IJMS

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“…The current study has several limitations, particularly the lack of a functional assessment of the intestinal graft. It would have been interesting to assess the functional mucosal recovery, with respect to the absorptive and barrier function as altered permeability is a hallmark of intestinal ischemia-reperfusion [41, 44]. In addition, the follow-up time was rather short and does not allow for prognostic considerations related to any of the findings.…”

Section: Discussionmentioning

confidence: 99%

Mucosal Recovery after Intestinal Transplantation in the Rat: A Sequential Histological and Molecular Assessment

et al. 2022

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Introduction Intestinal cold ischemia and subsequent reperfusion during transplantation result in various degrees of mucosal injury ranging from mild edema to extensive mucosal loss. Mucosal barrier impairment favours bacterial translocation and fluid loss and raises nutritional challenges. The injured intestine also releases proinflammatory mediators and upregulates various epitopes towards an inflammatory phenotype. We studied the process of mucosal injury and repair during the early period after intestinal transplantation from a histological and molecular standpoint. Materials and Methods Adult Sprague Dawley rats were used as donors and recipients. Donor intestines were perfused and stored in saline for 3 hours, then transplanted heterotopically using microvascular anastomoses. Intestinal graft segments were obtained after 20 minutes, 6 hours, 12 hours, and 24 hours after reperfusion. Histology studies (goblet cell count, morphometry), immunofluorescence and western blot for several tight junction proteins, apoptosis and inflammation related proteins were performed. Results Cold storage led to extensive epithelial detachment, whereas reperfusion resulted in extensive villus loss (about 60 % of the initial length) and goblet cell numbers were drastically reduced. Over the first 24 hours, gradual morphologic and molecular recovery was noted, although several molecular alterations persisted (increased apoptosis and inflammation, altered expression of several tight junctions). Conclusions The current data suggest that a near-complete morphologic recovery from a moderate mucosal injury occurs within the first 24 hours after intestinal transplantation. However, several molecular alterations persist and need to be considered when designing intestinal transplant experiments and choosing sampling and endpoints.

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“…It is a pleiotropic compound with anti-tumor and anti-microbial activities, as widely demonstrated in experimental models [ 231 , 232 , 233 ]. Data obtained in animal models showed a protective activity of sulforaphane in IRI affecting different tissues, including kidney [ 234 ], retina [ 235 ] and intestine [ 236 , 237 ].…”

Section: Nrf2 Signaling Pathway and Ischemic Strokementioning

confidence: 99%

The Nrf2 Pathway in Ischemic Stroke: A Review

Farina

Vieira

Buttari³

et al. 2021

Molecules

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Ischemic stroke, characterized by the sudden loss of blood flow in specific area(s) of the brain, is the leading cause of permanent disability and is among the leading causes of death worldwide. The only approved pharmacological treatment for acute ischemic stroke (intravenous thrombolysis with recombinant tissue plasminogen activator) has significant clinical limitations and does not consider the complex set of events taking place after the onset of ischemic stroke (ischemic cascade), which is characterized by significant pro-oxidative events. The transcription factor Nuclear factor erythroid 2-related factor 2 (Nrf2), which regulates the expression of a great number of antioxidant and/or defense proteins, has been pointed as a potential pharmacological target involved in the mitigation of deleterious oxidative events taking place at the ischemic cascade. This review summarizes studies concerning the protective role of Nrf2 in experimental models of ischemic stroke, emphasizing molecular events resulting from ischemic stroke that are, in parallel, modulated by Nrf2. Considering the acute nature of ischemic stroke, we discuss the challenges in using a putative pharmacological strategy (Nrf2 activator) that relies upon transcription, translation and metabolically active cells in treating ischemic stroke patients.

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Sulforaphane Elicits Protective Effects in Intestinal Ischemia Reperfusion Injury

Cited by 7 publications

References 51 publications

Sulforaphane Attenuates Neutrophil ROS Production, MPO Degranulation and Phagocytosis, but Does Not Affect NET Formation Ex Vivo and In Vitro

Sulforaphane Attenuates Neutrophil ROS Production, MPO Degranulation and Phagocytosis, but Does Not Affect NET Formation Ex Vivo and In Vitro

Mucosal Recovery after Intestinal Transplantation in the Rat: A Sequential Histological and Molecular Assessment

The Nrf2 Pathway in Ischemic Stroke: A Review

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