Effect of N-Acetylserotonin on TLR-4 and MyD88 Expression during Intestinal Ischemia-Reperfusion in a Rat Model

Sukhotnik, Igor; Shahar, Y. Ben; Halabi, Salim; Bitterman, Noemi; Dorfman, Tatiana; Pollak, Yulia; Coran, Arnold G.; Bitterman, Arie

doi:10.1055/s-0037-1618593

Cited by 13 publications

(8 citation statements)

References 33 publications

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“…Furthermore, AS-IV, bicyclol, SAB, and dioscin all played protective roles in cerebral IRI by inhibiting the TLR4/MyD88/TRAF6/NF-κB axis (Zhang et al, 2013;Tao et al, 2015;Wang et al, 2016;Li M. et al, 2017; Figure 4). Additionally, the latest research showed that TRAF6 was also involved in the regulation of aloin and NAS preconditioning to reduce liver and intestinal IRI, respectively (Du et al, 2019;Sukhotnik et al, 2019; Figure 4). The above research indicated that TRAFs have received much attention in the treatment of IRI, and new treatment methods and related mechanisms have been continuously discovered.…”

Section: Perspectivesmentioning

confidence: 99%

“…Meaningfully, many drugs or compounds can reduce cerebral IRI targeting the axis, including Astragaloside IV (AS-IV), bicyclol, salvianolic acid B (SAB), and dioscin ( Zhang et al, 2013 ; Tao et al, 2015 ; Wang et al, 2016 ; Li M. et al, 2017 ; Figure 4 ). Moreover, aloin and N-Acetylserotonin (NAS) were respectively involved in the regulating of liver and intestinal IRI by targeting TRAF6 ( Du et al, 2019 ; Sukhotnik et al, 2019 ; Figure 4 ), which provides targets for clinical treatment of liver and intestinal IRI-related diseases. In addition, miRNA-based treatments for IRI are very popular in recent years ( Huang Z. et al, 2019 ; Liang et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

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Roles of TRAFs in Ischemia-Reperfusion Injury

Wei

Lin

Zhong

et al. 2020

Front. Cell Dev. Biol.

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Tumor necrosis factor receptor-associated factor (TRAF) proteins are a family of signaling molecules that function downstream of multiple receptor signaling pathways, and they play a pivotal role in the regulation of intracellular biological progresses. These TRAFdependent signaling pathways and physiological functions have been involved in the occurrence and progression of ischemia-reperfusion injury (IRI), which is a common pathophysiological process that occurs in a wide variety of clinical events, including ischemic shock, organ transplantation, and thrombolytic therapy, resulting in a poor prognosis and high mortality. IRI occurs in multiple organs, including liver, kidney, heart, lung, brain, intestine, and retina. In recent years, mounting compelling evidence has confirmed that the genetic alterations of TRAFs can cause subversive phenotype changes during IRI of those organs. In this review, based on current knowledge, we summarized and analyzed the regulatory effect of TRAFs on the IRI of various organs, providing clear direction and a firm theoretical basis for the development of treatment strategies to manipulate TRAF proteins or TRAF-dependent signaling pathways in IRI-related diseases.

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Section: Perspectivesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Roles of TRAFs in Ischemia-Reperfusion Injury

Wei

Lin

Zhong

et al. 2020

Front. Cell Dev. Biol.

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“…While 5-HT predominantly exerts proinflammatory effects, emerging evidence points to the anti-inflammatory and anti-oxidant effects of its endogenous fatty acid-conjugates, Nacyl 5-HTs, present in the gut [38][39][40][41]138]. Our laboratory uncovered that docosahexaenoylserotonin (DHA-5-HT), the conjugate of 5-HT with the n-3 poly unsaturated long chain fatty acid (LC PUFA) DHA, has anti-inflammatory effects both in mouse macrophages as well as in human peripheral blood mononuclear cells (PBMCs), by attenuating release of key inflammatory mediators [40,41].…”

Section: Fatty Acid-5-ht Conjugates With Immune-modulatory and Anti-omentioning

confidence: 99%

“…Furthermore, N-acyl-5-HTs with varying fatty acid moieties were reported to exert anti-inflammatory, anti-oxidant, and neuroprotective effects in a number of in vivo animal disease models [38,39,[142][143][144][145]. In an inflammatory in vivo gut model, the SCFA conjugate of 5-HT, N-acetyl-5-HT (also called NAS), has been shown to prevent gut mucosal damage and inhibit programmed cell death following intestinal ischemia-reperfusion (IR) in rats [38].…”

Section: Fatty Acid-5-ht Conjugates With Immune-modulatory and Anti-omentioning

confidence: 99%

“…These include the well-known group of the Nacyl-ethanolamides [31][32][33][34][35][36] and 2-acyl glycerols [37], of which several are classified as endocannabinoids. More recently, fatty acid conjugates with serotonin (5-HT) emerged as a class of molecules with immune-modulatory and anti-oxidant effects [38,39]. Of these, the 5-HT acyl-conjugates with long chain fatty acids (LCFAs) are present in the GI tract and the available evidence points towards a role in modulating immune responses and relevance for inflammatory pathologies of gut [40,41].…”

Section: Introductionmentioning

confidence: 99%

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The Intestinal Fatty Acid-Enteroendocrine Interplay, Emerging Roles for Olfactory Signaling and Serotonin Conjugates

Meijerink

2021

Molecules

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Intestinal enteroendocrine cells (EECs) respond to fatty acids from dietary and microbial origin by releasing neurotransmitters and hormones with various paracrine and endocrine functions. Much has become known about the underlying signaling mechanisms, including the involvement of G-protein coupled receptors (GPCRs), like free fatty acids receptors (FFARs). This review focusses on two more recently emerging research lines: the roles of odorant receptors (ORs), and those of fatty acid conjugates in gut. Odorant receptors belong to a large family of GPCRs with functional roles that only lately have shown to reach beyond the nasal-oral cavity. In the intestinal tract, ORs are expressed on serotonin (5-HT) and glucagon-like-peptide-1 (GLP-1) producing enterochromaffin and enteroendocrine L cells, respectively. There, they appear to function as chemosensors of microbiologically produced short-, and branched-chain fatty acids. Another mechanism of fatty acid signaling in the intestine occurs via their conjugates. Among them, conjugates of unsaturated long chain fatty acids and acetate with 5-HT, N-acyl serotonins have recently emerged as mediators with immune-modulatory effects. In this review, novel findings in mechanisms and molecular players involved in intestinal fatty acid biology are highlighted and their potential relevance for EEC-mediated signaling to the pancreas, immune system, and brain is discussed.

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Retracted: Overexpression of microRNA‐590‐3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF‐κB signaling pathway by binding to RIPK1

Zhao

Jiang

Wang

et al. 2018

J of Cellular Biochemistry

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Ischemic heart disease is widely considered as a major health threat, which causes a high number of deaths every year worldwide. Much evidence has shown that oxidative stress (OS) is implicated in the pathogenesis of ischemiareperfusion injury (IRI). This study aims to evaluate the effect of miR-590-3p on the OS of IRI mice through the nuclear factor kappa-B (NF-κB) signaling pathway by targeting receptor-interacting protein kinase 1 (RIPK1). IRI mouse models were established for extracting myocardial tissues and isolating myocardial cells. The expression of inflammatory related-factors was detected by enzyme-linked immunosorbent assay, and superoxide dismutase (SOD) and malondialdehyde (MDA) in tissues were determined. Reverse transcription quantitative polymerase chain reaction and Western blot analysis were performed to assess the role of miR-590-3p in the expression of NF-κB-related factors and apoptosis-related factors. Besides, the regulatory effects of miR-590-3p on myocardial cell proliferation and apoptosis were also assessed. According to the obtained results, we found that IRI mice displayed higher expression of tumor necrosis factor-α, interleukin (IL)-6, and interferon-γ, lower expression of IL-10 in serum, a decreased SOD level, and an increased MDA level. In addition, RIPK1 was determined as a target gene of miR-590-3p. After transfection of overexpressed miR-590-3p or si-RIPK1, declined RIPK1, NF-κB, Toll-like receptor 4, caspase-3, FasL, p53, and c-myc levels, increased B-cell lymphoma-2 level, promoted cell proliferation, promoted cell cycle distribution and inhibited apoptosis of myocardial cells were found. Our study demonstrates that miR-590-3p can alleviate the OS of IRI mice through the inhibition of the RIPK1 and NF-κB signaling pathway. Thus, miR-590-3p represents a potential target for IRI repair. K E Y W O R D S microRNA-590-3p, myocardial ischemia/reperfusion injury, nuclear factor kappa-B (NF-κB), oxidative stress (OS), receptor-interacting protein kinase 1 (RIPK1) J Cell Biochem. 2019;120:3559-3573.wileyonlinelibrary.com/journal/jcb Overexpression of microRNA-590-3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF-κB signaling pathway by binding to RIPK1.

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Effect of N-Acetylserotonin on TLR-4 and MyD88 Expression during Intestinal Ischemia-Reperfusion in a Rat Model

Abstract: Treatment with NAS is associated with downregulation of TLR-4, MyD88, and TRAF6 expression along with a concomitant decrease in intestinal mucosal injury caused by intestinal IR in a rat.

Cited by 13 publications

References 33 publications

Roles of TRAFs in Ischemia-Reperfusion Injury

Roles of TRAFs in Ischemia-Reperfusion Injury

The Intestinal Fatty Acid-Enteroendocrine Interplay, Emerging Roles for Olfactory Signaling and Serotonin Conjugates

Retracted: Overexpression of microRNA‐590‐3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF‐κB signaling pathway by binding to RIPK1

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