Resveratrol efficiently improves pulmonary function via stabilizing mast cells in a rat intestinal injury model

Huang, Xiaolei; Zhao, Weicheng; Hu, Dan; Han, Xue; Wang, Hanbin; Yang, Jianyu; Yang, Xu; Li, Yuantao; Yao, Weifeng; Chen, Chaojin

doi:10.1016/j.lfs.2017.07.018

Cited by 18 publications

(14 citation statements)

References 38 publications

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“…And the neutrophil elastase and 8-isoprostane were detected using ELISA kits (Cayman Chemical). Superoxide dismutase (SOD) and myeloperoxidase (MPO) activities were measured according to our previous methods [ 16 ].…”

Section: Methodsmentioning

confidence: 99%

“…Immunohistochemical staining was performed in a previous study [ 16 ]. Liver tissue sections were deparaffinized, hydrated, and incubated at 4°C overnight with a p47 phox primary antibody (Cell Signaling Technology, Danvers, USA, diluted 1 : 500), followed by incubation with a horseradish peroxidase-coupled anti-rabbit IgG secondary antibody at room temperature for 2 hours and then colored with diaminobenzidine (DAB) for 3 minutes.…”

Section: Methodsmentioning

confidence: 99%

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Intravenous Anesthetic Protects Hepatocyte from Reactive Oxygen Species‐Induced Cellular Apoptosis during Liver Transplantation In Vivo

Yao

Han

Zhang

et al. 2018

Oxidative Medicine and Cellular Longevity

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Background Liver transplantation leads to liver ischemia/reperfusion (I/R) injury, resulting in early graft dysfunction and failure. Exacerbations of oxidative stress and inflammatory response are key processes in the development of liver I/R injury. Intravenous anesthetic propofol potent effects on free radical scavenging and protects livers against I/R injury. However, the role and mechanism of propofol-mediated hepatic protection in liver transplantation is poorly understood. The aim of this study was to evaluate the role of propofol postconditioning in the liver I/R injury after liver transplantation. Methods Forty-eight rats were randomly divided into six groups: rats receiving either sham operation or orthotopic autologous liver transplantation (OALT) in the absence or presence of propofol (high dose and low dose) postconditioning or intralipid control or VAS2870 (Nox2 special inhibitor). Eight hours after OALT or sham operation, parameters of organ injury, oxidative stress, inflammation, and NADPH-associated proteins were assessed. Results After OALT, severe liver pathological injury was observed that was associated with increases of serum AST and ALT, which were attenuated by propofol postconditioning. In addition, especially high dose of propofol postconditioning reduced TNF-α, IL-1β, IL-6, TLR4, and NF-κB inflammatory pathway, accompanied with decrease of neutrophil elastase activity, MPO activity, 8-isoprotane, p47phox and gp91phox protein expressions, and increase of SOD activity. Inhibition of Nox2 by VAS2870 conferred similar protective effects in liver transplantation. Conclusion Liver transplantation leads to severe inflammation and oxidative stress with NADPH oxidase activation. Propofol postconditioning reduces liver I/R injury after liver transplantation partly via inhibiting NADPH oxidase Nox2 and the subsequent inflammation and oxidative stress.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Intravenous Anesthetic Protects Hepatocyte from Reactive Oxygen Species‐Induced Cellular Apoptosis during Liver Transplantation In Vivo

Yao

Han

Zhang

et al. 2018

Oxidative Medicine and Cellular Longevity

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“…Chemo-induced neuropathy 230 Natural flavonoids Stimulated mast cell 231,232 Resveratrol Oxidative stress Intestinal ischemia/reperfusion (IIR)-induced acute lung injury 233…”

Section: Target Pathology Referencementioning

confidence: 99%

Mast cell‐neural interactions contribute to pain and itch

Gupta

Harvima

2018

Immunological Reviews

205

189

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Mast cells are best recognized for their role in allergy and anaphylaxis, but increasing evidence supports their role in neurogenic inflammation leading to pain and itch. Mast cells act as a "power house" by releasing algogenic and pruritogenic mediators, which initiate a reciprocal communication with specific nociceptors on sensory nerve fibers. Consequently, nerve fibers release inflammatory and vasoactive neuropeptides, which in turn activate mast cells in a feedback mechanism, thus promoting a vicious cycle of mast cell and nociceptor activation leading to neurogenic inflammation and pain/pruritus. Mechanisms underlying mast cell differentiation, activation, and intercellular interactions with inflammatory, vascular, and neural systems are deeply influenced by their microenvironment, imparting enormous heterogeneity and complexity in understanding their contribution to pain and pruritus. Neurogenic inflammation is central to both pain and pruritus, but specific mediators released by mast cells to promote this process may vary depending upon their location, stimuli, underlying pathology, gender, and species. Therefore, in this review, we present the contribution of mast cells in pathological conditions, including distressing pruritus exacerbated by psychologic stress and experienced by the majority of patients with psoriasis and atopic dermatitis and in different pain syndromes due to mastocytosis, sickle cell disease, and cancer.

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“…After 60 min of occlusion, intestinal blood flow was restored by removing the microvascular clamp. This I/R regimen (60-min ischemia followed by 180-min reperfusion) was chosen because this time course provoked the most severe intestinal inflammation and oxidative stress in our previous study [16]. Sham-operated mice were subjected to identical surgical interventions including laparotomy and vascular microdissection for the same operation period without SMA occlusion.…”

Section: Intestinal Ischemia/reperfusion Modelmentioning

confidence: 99%

MicroRNA files in the prevention of intestinal ischemia/reperfusion injury by hydrogen rich saline

et al. 2020

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Background: Hydrogen-rich saline (HRS) has been proven effective against ischemia/reperfusion (I/R) injury. However, knowledge on the underlying signaling events remain poor. Having recent highlight of microRNAs (miRNAs) in mediating intestinal I/R injury, we hypothesized that HRS may protect intestine against I/R injury by regulating miRNAs. Method: Mice were given intraperitoneal injection of saline or HRS once daily for five consecutive days before undergoing intestinal I/R that was induced by 60-min ischemia followed by 180-min reperfusion of superior mesenteric artery. The intestine was collected for histopathological assay, miRNA microarray profiling, Real-Time PCR, and Western blotting. Next, miR-199a-3p mimics or inhibitors were transfected into IEC-6 cells to explore the relationship between HRS treatment and miR-199a-3p. Results: I/R-induced mucosal injury and epithelial cells apoptosis were attenuated by HRS pretreatment. A total of 64 intestinal I/R-responsive miRNAs were altered significantly by HRS pretreatment, in which we validated four novel miRNAs with top significance by was drastically increased by I/R but reduced by HRS. Computational analysis predicts insulin-like growth factor (IGF)-1, mammalian target of rapamycin (mTOR), and phosphoinositide-3-kinase (PI3K) regulatory subunit 1 as targets of miR-199a-3p, suggesting involvement of the pro-survival pathway, IGF-1/PI3K/Akt/mTOR. In in vitro experiment, HRS treatment reduced miR-199a-3p level, increase IGF-1, PI3K and mTOR mRNA expression, restore IEC-6 cells viability, and this protective effects were reversed under miR-199a-3p mimics treatment. Conclusion: Collectively, miR-199a-3p may serve a key role in the anti-apoptotic mechanism of HRS that contributes to its protection of the intestine against I/R injury.

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Resveratrol efficiently improves pulmonary function via stabilizing mast cells in a rat intestinal injury model

Cited by 18 publications

References 38 publications

Intravenous Anesthetic Protects Hepatocyte from Reactive Oxygen Species‐Induced Cellular Apoptosis during Liver Transplantation In Vivo

Intravenous Anesthetic Protects Hepatocyte from Reactive Oxygen Species‐Induced Cellular Apoptosis during Liver Transplantation In Vivo

Mast cell‐neural interactions contribute to pain and itch

MicroRNA files in the prevention of intestinal ischemia/reperfusion injury by hydrogen rich saline

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