Sulforaphane Ameliorates the Liver Injury of Traumatic Hemorrhagic Shock Rats

Guan, Zhihui; Zhou, Lingmin; Zhang, Yu; Chen, Zhidong; Shao, Feifei

doi:10.1016/j.jss.2021.05.004

Cited by 6 publications

(7 citation statements)

References 27 publications

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“…Our study has the following several limitations. First, the study only chose one feasible dose of SFN based on the previous studies (13,25). Thus, its safe and effective dose range requires further investigation.…”

Section: Discussionmentioning

confidence: 99%

“…In 2013, Jensen et al Based on the research evidence mentioned previously, the present study was designed to confirm the potential protective effects of SFN treatment on systemic lung IR injury resulted from CA and resuscitation. First, a dose of 2 mg/kg of SFN was chosen based on the previous several studies and the principle of dose conversion between the animals (13,25,26). Second, the SFN was given after restoring spontaneous circulation according to the earliest timing of postresuscitation care (27,28).…”

Section: Discussionmentioning

confidence: 99%

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Sulforaphane Alleviates Postresuscitation Lung Pyroptosis Possibly via Activating the Nrf2/Ho-1 Pathway

Li,

Yang,

Xie

et al. 2023

Shock

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Introduction Sulforaphane (SFN), known as the activator of the nuclear factor E2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway, has been proven to protect the lung against various pathological stimuli. The present study aimed to investigate the effect of SFN on lung injury induced by systemic ischemia reperfusion following cardiac arrest and resuscitation. Methods After animal preparation, twenty-four pigs were randomly divided into Sham group (n = 6), cardiopulmonary resuscitation group (CPR, n = 9), or CPR + SFN group (n = 9). The experimental model was then established by 10 min of cardiac arrest followed by 6 min of CPR. Once spontaneous circulation was achieved, a dose of 2 mg/kg of SFN diluted in 20 ml of saline was intravenously infused with a duration of 5 min. During 4 h of observation after resuscitation, extravascular lung water index (ELWI), pulmonary vascular permeability index (PVPI), and oxygenation index (OI) were regularly evaluated. At 24 h after resuscitation, lung tissues were harvested to evaluate the score of lung histopathological injury, the activity of superoxide dismutase (SOD), the contents of malondialdehyde (MDA), interleukin-1β (IL-1β), and interleukin-18 (IL-18), and the expression levels of NOD-like receptor pyrin domain 3 (NLRP3), cleaved caspase 1, gasdermin D (GSDMD), GSDMD N-terminal (GSDMD-N), Nrf2, and HO-1. Results During CPR, spontaneous circulation was achieved in 6 and 7 pigs in the CPR and CPR + SFN groups, respectively. After resuscitation, the indicators of lung injury (ELWI, PVPI, and OI) were all better in the CPR + SFN group than in the CPR group, in which the differences in ELWI and PVPI at 2, and 4 h after resuscitation were significant between the two groups. In addition, SFN significantly reduced lung injury score, improved oxidative imbalance (SOD, MDA), decreased pyroptosis-related proinflammatory cytokines (IL-1β, IL-18), downregulated pyroptosis-related proteins (NLRP3, cleaved caspase 1, GSDMD, GSDMD-N), and activated the Nrf2/HO-1 pathway when compared to the CPR group. Conclusions SFN produced effective post-resuscitation lung protection through alleviating lung pyroptosis possibly via activating the Nrf2/HO-1 pathway in pigs.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Sulforaphane Alleviates Postresuscitation Lung Pyroptosis Possibly via Activating the Nrf2/Ho-1 Pathway

Li,

Yang,

Xie

et al. 2023

Shock

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“…Further research on renal inflammation in rats has included folic acid-induced acute renal injury [ 52 ] and cisplatin-induced nephropathy where the expression of pro-inflammatory cytokine (TNF-α) and nuclear factor κB (NF-κB) were suppressed [ 53 ]. Other inflammation models in rats for sulforaphane research were cancer-induced bone pain [ 54 ], carrageenan-induced oedema [ 55 ], the traumatic haemorrhagic shock model [ 56 ], chromium-induced lung injury [ 57 ], arsenic-induced nephrotoxicity [ 58 ], ioversol-induced nephropathy [ 59 ], the neuroinflammation and spatial learning model [ 60 ], age-related renal injury in rats [ 61 ], anti-nociceptive and anti-inflammatory effects on a sciatic endometriosis rat model [ 62 ], and chronic renal allograft dysfunction [ 63 ].…”

Section: Anti-inflammatory Effects In Vivomentioning

confidence: 99%

Anti-Inflammatory Therapeutic Mechanisms of Isothiocyanates: Insights from Sulforaphane

Habtemariam

2024

Biomedicines

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Isothiocyanates (ITCs) belong to a group of natural products that possess a highly reactive electrophilic -N=C=S functional group. They are stored in plants as precursor molecules, glucosinolates, which are processed by the tyrosinase enzyme upon plant tissue damage to release ITCs, along with other products. Isolated from broccoli, sulforaphane is by far the most studied antioxidant ITC, acting primarily through the induction of a transcription factor, the nuclear factor erythroid 2–related factor 2 (Nrf2), which upregulates downstream antioxidant genes/proteins. Paradoxically, sulforaphane, as a pro-oxidant compound, can also increase the levels of reactive oxygen species, a mechanism which is attributed to its anticancer effect. Beyond highlighting the common pro-oxidant and antioxidant effects of sulforaphane, the present paper was designed to assess the diverse anti-inflammatory mechanisms reported to date using a variety of in vitro and in vivo experimental models. Sulforaphane downregulates the expression of pro-inflammatory cytokines, chemokines, adhesion molecules, cycloxyhenase-2, and inducible nitric oxide synthase. The signalling pathways of nuclear factor κB, activator protein 1, sirtuins 1, silent information regulator sirtuin 1 and 3, and microRNAs are among those affected by sulforaphane. These anti-inflammatory actions are sometimes due to direct action via interaction with the sulfhydryl structural moiety of cysteine residues in enzymes/proteins. The following are among the topics discussed in this paper: paradoxical signalling pathways such as the immunosuppressant or immunostimulant mechanisms; crosstalk between the oxidative and inflammatory pathways; and effects dependent on health and disease states.

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“…demonstrated that sulforaphane, a potential immune modulator, could protect the liver from HS-induced inflammation storm by decreasing the secretion of TNF-α, MCP-1, KC/CXCL1, IL-6, and IL-10 and abolishing neutrophil infiltration in kupffer cells ( 126 ). Moreover, in a mouse HS model, sulforaphane administration reduced lung and liver injury via down-regulating pro-inflammatory cytokines, such as TNF-α, COX-2, iNOS, and IL-1β ( 127 , 128 ).…”

Section: New Insights Into Hs Therapeutics With Innate Immune Regulationmentioning

confidence: 99%

Innate immunity and immunotherapy for hemorrhagic shock

Huang

Gao²,

Yao

et al. 2022

Front. Immunol.

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Hemorrhagic shock (HS) is a shock result of hypovolemic injury, in which the innate immune response plays a central role in the pathophysiology ofthe severe complications and organ injury in surviving patients. During the development of HS, innate immunity acts as the first line of defense, mediating a rapid response to pathogens or danger signals through pattern recognition receptors. The early and exaggerated activation of innate immunity, which is widespread in patients with HS, results in systemic inflammation, cytokine storm, and excessive activation of complement factors and innate immune cells, comprised of type II innate lymphoid cells, CD4+ T cells, natural killer cells, eosinophils, basophils, macrophages, neutrophils, and dendritic cells. Recently, compelling evidence focusing on the innate immune regulation in preclinical and clinical studies promises new treatment avenues to reverse or minimize HS-induced tissue injury, organ dysfunction, and ultimately mortality. In this review, we first discuss the innate immune response involved in HS injury, and then systematically detail the cutting-edge therapeutic strategies in the past decade regarding the innate immune regulation in this field; these strategies include the use of mesenchymal stem cells, exosomes, genetic approaches, antibody therapy, small molecule inhibitors, natural medicine, mesenteric lymph drainage, vagus nerve stimulation, hormones, glycoproteins, and others. We also reviewed the available clinical studies on immune regulation for treating HS and assessed the potential of immune regulation concerning a translation from basic research to clinical practice. Combining therapeutic strategies with an improved understanding of how the innate immune system responds to HS could help to identify and develop targeted therapeutic modalities that mitigate severe organ dysfunction, improve patient outcomes, and reduce mortality due to HS injury.

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Sulforaphane Ameliorates the Liver Injury of Traumatic Hemorrhagic Shock Rats

Cited by 6 publications

References 27 publications

Sulforaphane Alleviates Postresuscitation Lung Pyroptosis Possibly via Activating the Nrf2/Ho-1 Pathway

Sulforaphane Alleviates Postresuscitation Lung Pyroptosis Possibly via Activating the Nrf2/Ho-1 Pathway

Anti-Inflammatory Therapeutic Mechanisms of Isothiocyanates: Insights from Sulforaphane

Innate immunity and immunotherapy for hemorrhagic shock

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