Category: 321673-30-7

Kwon, Sun-Young published the artcileMediatory roles of leukotriene B₄ receptors in LPS-induced endotoxic shock, Related Products of amides-buliding-blocks, the publication is Scientific Reports (2019), 9(1), 1-8, database is CAplus and MEDLINE.

Sepsis, a systemic inflammatory response syndrome caused by infection, is the most common disease in patients treated in intensive care units. Endotoxic shock, the most critical form of sepsis, is caused by gram-neg. bacterial infection. However, the detailed mechanism of endotoxic shock remains unclear. In the present study, we observed that the production of leukotriene B₄ (LTB₄) and 12(S)-hydroxyeicosatetraenoic acid (HETE), inflammatory lipid mediators acting on LTB₄ receptors (BLT1 and BLT2), was significantly upregulated in peritoneal lavage fluid (PF) and serum from an LPS-induced endotoxic shock mouse model. Furthermore, BLT1/2-dependent signaling pathways mediated the expression of IL-17, IL-6, and IL-1β, key cytokines for the development of endotoxic shock, via NF-κB activation in the LPS-induced endotoxic shock mouse model. Addnl., inhibition of BLT1/2 significantly attenuated inflammation and tissue damage associated with endotoxic shock and enhanced the survival rate of mice with this inflammatory complication. Together, these results suggest that LTB₄ receptors play critical mediatory roles in the development of endotoxic shock. Our findings point to LTB₄ receptors as potential therapeutic targets for the treatment of endotoxic shock.

Scientific Reports published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Related Products of amides-buliding-blocks.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Arbizzani, Federica published the artcileIncreasing ergosterol levels delays formin-dependent assembly of F-actin cables and disrupts division plane positioning in fission yeast, Safety of [(2-Hexylcyclopentylidene)amino]thiourea, the publication is Journal of Cell Science (2019), 132(13), jcs227447, database is CAplus and MEDLINE.

In most eukaryotes, cytokinesis is mediated by the constriction of a contractile acto-myosin ring (CR), which promotes the ingression of the cleavage furrow. Many components of the CR interact with plasma membrane lipids suggesting that lipids may regulate CR assembly and function. Although there is clear evidence that phosphoinositides play an important role in cytokinesis, much less is known about the role of sterols in this process. Here, we studied how sterols influence division plane positioning and CR assembly in fission yeast.We show that increasing ergosterol levels in the plasma membrane blocks the assembly of F-actin cables from cytokinetic precursor nodes, preventing their compaction into a ring. Abnormal F-actin cables form after a delay, leading to randomly placed septa. Since the formin Cdc12 was detected on cytokinetic precursors and the phenotype can be partially rescued by inhibiting the Arp2/3 complex, which competes with formins for F-actin nucleation, we propose that ergosterol may inhibit formin dependent assembly of F-actin cables from cytokinetic precursors.

Journal of Cell Science published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Safety of [(2-Hexylcyclopentylidene)amino]thiourea.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Simons, Sami O. published the artcileMontelukast for bronchiolitis obliterans syndrome after lung transplantation, Safety of [(2-Hexylcyclopentylidene)amino]thiourea, the publication is Chest (2012), 141(1), 275-276, database is CAplus and MEDLINE.

A review. A polemic in response to Todd and Palmer (Chest 2011, 140, 2, 502-508) is given. In their study, Todd and Palmer provided an excellent overview of the pathogenesis of bronchiolitis obliterans syndrome after lung transplantation, placing emphasis on future clin. translational treatment directions. Although their review is thorough, the authors have missed one important translational development, namely the leukotriene B4 pathway in the pathophysiol. of bronchiolitis obliterans syndrome after lung transplantation.

Chest published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C13H12BClO3, Safety of [(2-Hexylcyclopentylidene)amino]thiourea.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Ramalho, Theresa published the artcileLeukotriene-B4 modulates macrophage metabolism and fat loss in type 1 diabetic mice, Product Details of C12H23N3S, the publication is Journal of Leukocyte Biology (2019), 106(3), 665-675, database is CAplus and MEDLINE.

Serum levels of leukotriene-B4 (LTB4) are increased in type 1 diabetes (T1D) and it mediates systemic inflammation and macrophage reprogramming associated with this condition. Herein, investigated the involvement of LTB4 in adiposity loss, hyperlipidemia, and changes in macrophage metabolism in a mouse model of streptozotocin-induced T1D. LTB4 receptor (BLT1) antagonist u75302 was employed to block LTB4 effects. As expected, hypoinsulinemia in T1D was associated with hyperglycemia, low levels of glucagon, hyperlipidemia, significant body fat loss, and increased white adipose tissue expression of Fgf21, a marker for lipolysis. With the exception of hyperglycemia and hypoglucagonemia, blockade of LTB4 signaling reverted these parameters in T1D mice. Along with hyperlipidemia, macrophages from T1D mice exhibited higher lipid uptake and accumulation. These cells also had enhanced glycolysis and oxidative metabolism and these parameters were dependent on the mitochondrial uncoupling respiration, as evidenced by elevated expression of oxidation markers carnitine palmitoyltransferase and uncoupling protein 1. Interestingly, all these parameters were at least partially reverted in T1D mice treated with u75302. Altogether, these findings suggest that in T1D mice LTB4/BLT1 is involved in the fat loss, hyperlipidemia, and increased macrophage lipid uptake and metabolism with an important involvement of mitochondrial uncoupling activity. These previously unrecognized LTB4/BLT1 functions may be explored in future to therapeutically alleviate severity of hyperlipidemia and systemic inflammation in T1D.

Journal of Leukocyte Biology published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Product Details of C12H23N3S.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Madeira, Mila F. M. published the artcileThe role of 5-lipoxygenase in Aggregatibacter actinomycetemcomitans-induced alveolar bone loss, Quality Control of 321673-30-7, the publication is Journal of Clinical Periodontology (2017), 44(8), 793-802, database is CAplus and MEDLINE.

Leukotrienes (LTs) are pro-inflammatory lipid mediators formed by the enzyme 5-lipoxygenase (5-LO). The involvement of 5-LO metabolites in periodontal disease (PD) is not well defined. This study aimed to assess the role of 5-LO in exptl. PD induced by Aggregatibacter actinomycetemcomitans (Aa). In vivo experiments were carried out using SV129 wild-type (WT) and 5-LO-deficient (5lo^-/-) mice inoculated with Aa. Osteoclasts were stimulated in vitro with AaLPS in the presence or not of selective inhibitors of the 5-LO pathway, or LTB4 or platelet-activating factor (PAF), as PAF has already been shown to increase osteoclast activity. In 5lo^-/- mice, there were no loss of alveolar bone and less TRAP-pos. osteoclasts in periodontal tissues, after Aa inoculation, despite local production of TNF-α and IL-6. The differentiation and activity of osteoclasts stimulated with AaLPS were diminished in the presence of BLT1 antagonist or 5-LO inhibitor, but not in the presence of cysteinyl leukotriene receptor antagonist. The osteoclast differentiation induced by PAF was impaired by the BLT1 antagonism. In conclusion, LTB4 but not CysLTs is important for Aa-induced alveolar bone loss. Overall, LTB4 affects osteoclast differentiation and activity and is a key intermediate of PAF-induced osteoclastogenesis.

Journal of Clinical Periodontology published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Quality Control of 321673-30-7.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Pazos, Michael A. published the artcileDistinct Cellular Sources of Hepoxilin A₃ and Leukotriene B₄ Are Used To Coordinate Bacterial-Induced Neutrophil Transepithelial Migration, Safety of [(2-Hexylcyclopentylidene)amino]thiourea, the publication is Journal of Immunology (2015), 194(3), 1304-1315, database is CAplus and MEDLINE.

Neutrophilic infiltration is a leading contributor to pathol. in a number of pulmonary disease states, including cystic fibrosis. Hepoxilin A₃ (HXA₃) is a chemotactic eicosanoid shown to mediate the transepithelial passage of neutrophils in response to infection in several model systems and at multiple mucosal surfaces. Another well-known eicosanoid mediating general neutrophil chemotaxis is leukotriene B₄ (LTB₄). We sought to distinguish the roles of each eicosanoid in the context of infection of lung epithelial monolayers by Pseudomonas aeruginosa. Using human and mouse in vitro transwell model systems, we used a combination of biosynthetic inhibitors, receptor antagonists, as well as mutant sources of neutrophils to assess the contribution of each chemoattractant in driving neutrophil transepithelial migration. We found that following chemotaxis to epithelial-derived HXA₃ signals, neutrophil-derived LTB₄ is required to amplify the magnitude of neutrophil migration. LTB₄ signaling is not required for migration to HXA₃ signals, but LTB₄ generation by migrated neutrophils plays a significant role in augmenting the initial HXA₃-mediated migration. We conclude that HXA₃ and LTB₄ serve independent roles to collectively coordinate an effective neutrophilic transepithelial migratory response.

Journal of Immunology published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Safety of [(2-Hexylcyclopentylidene)amino]thiourea.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Stanke-Labesque, Francoise published the artcileLeukotriene B₄ pathway activation and atherosclerosis in obstructive sleep apnea, Product Details of C12H23N3S, the publication is Journal of Lipid Research (2012), 53(9), 1944-1951, database is CAplus and MEDLINE.

Leukotriene B₄ (LTB₄) production increases in obstructive sleep apnea syndrome (OSA) and is linked to early vascular remodeling, the mechanism of which is unknown. The objective of this study was to to determine the mol. mechanisms of LTB₄ pathway activation in polymorphonuclear cells (PMNs) and early vascular remodeling in OSA and the specific contribution of intermittent hypoxia (IH). PMNs were isolated from 120 OSA patients and 33 healthy subjects and used for measurements of LTB₄ production, determination of mRNA and protein expression levels, or exposed for four cycles of in vitro IH. PMNs derived from OSA patients exhibited increased LTB₄ production, for which apnea-hypopnea index was an independent predictor (P = 0.042). 5-Lipoxygenase-activating protein (FLAP) mRNA and protein increased significantly in PMNs from OSA patients vs. controls and were associated with carotid luminal diameter and intima-media thickness. LTB₄ (10 ng/mL) increased IL-6 (P = 0.006) and MCP-1 (P = 0.002) production in OSA patient monocytes. In vitro exposure of PMNs from controls to IH enhanced FLAP mRNA levels (P = 0.027) and induced a 2.7-fold increase (P = 0.028) in LTB₄ secretion compared with PMNs exposed to normoxia. In conclusion, upregulation of FLAP in PMNs in response to IH may participate in early vascular remodeling in OSA patients, suggesting FLAP as a potential therapeutic target for the cardiovascular morbidity associated with OSA.

Journal of Lipid Research published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C6H5NO, Product Details of C12H23N3S.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Nieland, Thomas J. F. published the artcileDiscovery of chemical inhibitors of the selective transfer of lipids mediated by the HDL receptor SR-BI, Recommanded Product: [(2-Hexylcyclopentylidene)amino]thiourea, the publication is Proceedings of the National Academy of Sciences of the United States of America (2002), 99(24), 15422-15427, database is CAplus and MEDLINE.

The high-d. lipoprotein (HDL) receptor, scavenger receptor, class B, type I (SR-BI), mediates both the selective uptake of lipids, mainly cholesterol esters, from HDL to cells and the efflux of cholesterol from cells to lipoproteins. The mechanism underlying these lipid transfers is distinct from classic receptor-mediated endocytosis, but it remains poorly understood. To investigate SR-BI’s mechanism of action and in vivo function, the authors developed a high-throughput screen to identify small mol. inhibitors of SR-BI-mediated lipid transfer in intact cells. The authors identified five compounds that in the low nanomolar to micromolar range block lipid transport (BLTs), both selective uptake and efflux. The effects of these compounds were highly specific to the SR-BI pathway, because they did not interfere with receptor-mediated endocytosis or with other forms of intracellular vesicular traffic. Surprisingly, all five BLTs enhanced, rather than inhibited, HDL binding by increasing SR-BI’s binding affinity for HDL (decreased dissociation rates). Thus, the BLTs provide strong evidence for a mechanistic coupling between HDL binding and lipid transport and may serve as a starting point for the development of pharmacol. useful modifiers of SR-BI activity and, thus, HDL metabolism

Proceedings of the National Academy of Sciences of the United States of America published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Recommanded Product: [(2-Hexylcyclopentylidene)amino]thiourea.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Kwak, Dong-Wook published the artcileLeukotriene B₄ receptors are necessary for the stimulation of NLRP3 inflammasome and IL-1β synthesis in neutrophil-dominant asthmatic airway inflammation, Safety of [(2-Hexylcyclopentylidene)amino]thiourea, the publication is Biomedicines (2021), 9(5), 535, database is CAplus and MEDLINE.

The stimulation of the NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome and IL-1β synthesis are associated with chronic respiratory diseases such as neutrophildominant severe asthma. Leukotriene B₄ (LTB₄) is a principal chemoattractant mol. for neutrophil recruitment, and its receptors BLT1 and BLT2 have been suggested to contribute to neutrophildominant asthmatic airway inflammation. However, the relationship between BLT1/2 and NLRP3 in neutrophil-dominant asthmatic airway inflammation has not been previously studied. In the present study, we investigated whether BLT1/2 play any roles in stimulating the NLRP3 inflammasome and IL-1βsynthesis. The blockade of BLT1 or BLT2 clearly suppressed the stimulation of the NLRP3 inflammasome and IL-1β synthesis in house dust mite (HDM)/lipopolysaccharide (LPS)-induced neutrophilic airway inflammation. The enzymes 5-lipoxygenase and 12-lipoxygenase, which catalyze the synthesis of BLT1/2 ligands [LTB₄, 12(S)-hydroxyeicosatetraenoic acid (12(S)-HETE), and 12-hydroxyheptadecatreinoic acid (12-HHT)], were also critically associated with the stimulation of NLRP3 and IL-1β synthesis. Together, our results suggest that the 5-/12-LOX-BLT1/2-linked cascade are necessary for the simulation of the NLRP3 inflammasome and IL-1β synthesis, thus contributing to HDM/LPS-induced neutrophil-dominant airway inflammation.

Biomedicines published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Safety of [(2-Hexylcyclopentylidene)amino]thiourea.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics

Min, Arim published the artcileBLT1-mediated O-GlcNAcylation is required for NOX2-dependent migration, exocytotic degranulation and IL-8 release of human mast cell induced by Trichomonas vaginalis-secreted LTB₄, Safety of [(2-Hexylcyclopentylidene)amino]thiourea, the publication is Microbes and Infection (2018), 20(6), 376-384, database is CAplus and MEDLINE.

Trichomonas vaginalis is a sexually-transmitted protozoan parasite that causes vaginitis and cervicitis. Although mast cell activation is important for provoking tissue inflammation during infection with parasites, information regarding the signaling mechanisms in mast cell activation and T. vaginalis infection is limited. O-linked N-acetylglucosamine (O-GlcNAc) is a post-translational modification of serine and threonine residues that functions as a critical regulator of intracellular signaling, regulated by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA). We investigated if O-GlcNAcylation was associated with mast cell activation induced by T. vaginalis-derived secretory products (TvSP). Modified TvSP collected from live trichomonads treated with the 5-lipooxygenase inhibitor AA861 inhibited migration of mast cells. This result suggested that mast cell migration was caused by stimulation of T. vaginalis-secreted leukotrienes. Using the BLT1 antagonist U75302 or BLT1 siRNA, we found that migration of mast cells was evoked via LTB₄ receptor (BLT1). Furthermore, TvSP induced protein O-GlcNAcylation and OGT expression in HMC-1 cells, which was prevented by transfection with BLT1 siRNA. TvSP-induced migration, ROS generation, CD63 expression and IL-8 release were significantly suppressed by pretreatment with OGT inhibitor ST045849 or OGT siRNA. These results suggested that BLT1-mediated OGlcNAcylation was important for mast cell activation during trichomoniasis.

Microbes and Infection published new progress about 321673-30-7. 321673-30-7 belongs to amides-buliding-blocks, auxiliary class Immunology/Inflammation,Scavenger receptor, name is [(2-Hexylcyclopentylidene)amino]thiourea, and the molecular formula is C12H23N3S, Safety of [(2-Hexylcyclopentylidene)amino]thiourea.

Referemce:
https://en.wikipedia.org/wiki/Amide,
Amide – an overview | ScienceDirect Topics