Category: 321673-30-7

Prado, Morgana K. B. published the artcileLeukotriene B₄ is essential for lung host defence and alpha-defensin-1 production during Achromobacter xylosoxidans infection, Related Products of amides-buliding-blocks, the publication is Scientific Reports (2017), 7(1), 1-13, database is CAplus and MEDLINE.

Leukotriene B₄ (LTB₄) is essential for host immune defense. It increases neutrophil recruitment, phagocytosis and pathogen clearance, and decreases edema and inflammasome activation. The host response and the role of LTB₄ during Achromobacter xylosoxidans infection remain unexplored. Wild-type (129sv) and LTB₄ deficient (Alox5^-/-) mice were intratracheally infected with A. xylosoxidans. Wild-type 129sv infected mice survived beyond the 8th day post-infection, exhibited increased levels of LTB₄ in the lung on the 1st day, while levels of PGE₂ increased on the 7th day post-infection. Infected Alox5^-/- mice showed impaired bacterial clearance, increased lung inflammation, and succumbed to the infection by the 7th day. We found that exogenous LTB₄ does not affect the phagocytosis of A. xylosoxidans by alveolar macrophages in vitro. However, treatment of infected animals with LTB₄ protected from mortality, by reducing the bacterial load and inflammation via BLT₁ signalling, the high affinity receptor for LTB₄. Of importance, we uncovered that LTB₄ induces gene and protein expression of α-defensin-1 during the infection. This mol. is essential for bacterial clearance and exhibits potent antimicrobial activity by disrupting A. xylosoxidans cell wall. Taken together, our data demonstrate a major role for LTB₄ on the control of A. xylosoxidans infection.

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

Li, Wenjing published the artcileDiesel exhaust particle promotes tumor lung metastasis via the induction of BLT1-mediated neutrophilic lung inflammation, COA of Formula: C12H23N3S, the publication is Cytokine+ (2018), 530-540, database is CAplus and MEDLINE.

BLT1, the primary functional receptor of Leukotriene B4 (LTB4), is involved in tissue inflammation by mediating leukocyte recruitment, and recently LTB4-dependent inflammation was reported to promote lung tumor growth. In this study, we found that DEP exposure led to acute lung inflammation, characterized by abundant infiltration of neutrophils and elevated lung levels in LTB4, as well as several pro-inflammatory cytokines and chemokines, including IL-1β, IL-6, TNF-α, CXCL1/2. BLT1 blockade by its specific antagonist U75302 significantly inhibited neutrophilic lung inflammation following DEP exposure. Importantly, BLT1 blockade before the onset of inflammation significantly reduced DEP-enhanced lung metastasis, which was associated with greatly decreased infiltrating neutrophils in lungs. Interestingly, BLT1 blockade after the occurrence of lung metastases had no effect on the magnitude of lung metastasis, suggesting that inhibition of BLT1-mediated lung inflammation was insufficient to suppress established metastatic tumor. Administration of BLT2 inhibitor LY255283 fails to inhibit DEP-induced lung inflammation and tumor metastasis. Collectively, our results demonstrate that DEP exposure causes BLT1-mediated lung neutrophilic inflammation, which is critical for tumor lung metastasis, and suggest that interruption of the LTB4-BLT1 axis could be useful for preventing PM_2.5-induced inflammation and subsequent susceptible to lung metastasis.

Cytokine+ 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, COA of Formula: C12H23N3S.

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

Peterson, Randall T. published the artcileSmall molecule developmental screens reveal the logic and timing of vertebrate development, HPLC of Formula: 321673-30-7, the publication is Proceedings of the National Academy of Sciences of the United States of America (2000), 97(24), 12965-12969, database is CAplus and MEDLINE.

Much has been learned about vertebrate development by random mutagenesis followed by phenotypic screening and by targeted gene disruption followed by phenotypic anal. in model organisms. Because the timing of many developmental events is critical, it would be useful to have temporal control over modulation of gene function, a luxury frequently not possible with genetic mutants. Here, the authors used synthetic small mols. from the DiverSet E obtained from Chembridge Corp., to demonstrate that small mols. capable of conditional gene product modulation can be identified through developmental screens in zebrafish. The authors have identified several small mols. that specifically modulate various aspects of vertebrate ontogeny, including development of the central nervous system, the cardiovascular system, the neural crest, and the ear. Several of the small mols. identified allowed the authors to dissect the logic of melanocyte and otolith development and to identify critical periods for these events. Small mols. identified in this way offer potential to dissect further these and other developmental processes and to identify novel genes involved in vertebrate development.

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, HPLC of Formula: 321673-30-7.

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

Zheng, Hao published the artcileDownregulation of COX-2 and CYP 4A signaling by isoliquiritigenin inhibits human breast cancer metastasis through preventing anoikis resistance, migration and invasion, Quality Control of 321673-30-7, the publication is Toxicology and Applied Pharmacology (2014), 280(1), 10-20, database is CAplus and MEDLINE.

Flavonoids exert extensive in vitro anti-invasive and in vivo anti-metastatic activities. Anoikis resistance occurs at multiple key stages of the metastatic cascade. Here, we demonstrate that isoliquiritigenin (ISL), a flavonoid from Glycyrrhiza glabra, inhibits human breast cancer metastasis by preventing anoikis resistance, migration and invasion through downregulating cyclooxygenase (COX)-2 and cytochrome P 450 (CYP) 4A signaling. ISL induced anoikis in MDA-MB-231 and BT-549 human breast cancer cells as evidenced by flow cytometry and the detection of caspase cleavage. Moreover, ISL inhibited the mRNA expression of phospholipase A2, COX-2 and CYP 4A and decreased the secretion of prostaglandin E₂ (PGE₂) and 20-hydroxyeicosatetraenoic acid (20-HETE) in detached MDA-MB-231 cells. In addition, it decreased the levels of phospho-PI3K (Tyr⁴⁵⁸), phospho-PDK (Ser²⁴¹) and phospho-Akt (Thr³⁰⁸). Conversely, the exogenous addition of PGE₂, WIT003 (a 20-HETE analog) and an EP4 agonist (CAY10580) or overexpression of constitutively active Akt reversed ISL-induced anoikis. ISL exerted the in vitro anti-migratory and anti-invasive activities, whereas the addition of PGE₂, WIT003 and CAY10580 or overexpression of constitutively active Akt reversed the in vitro anti-migratory and anti-invasive activities of ISL in MDA-MB-231 cells. Notably, ISL inhibited the in vivo lung metastasis of MDA-MB-231 cells, together with decreased intratumoral levels of PGE₂, 20-HETE and phospho-Akt (Thr³⁰⁸). In conclusion, ISL inhibits breast cancer metastasis by preventing anoikis resistance, migration and invasion via downregulating COX-2 and CYP 4A signaling. It suggests that ISL could be a promising multi-target agent for preventing breast cancer metastasis, and anoikis could represent a novel mechanism through which flavonoids may exert the anti-metastatic activities.

Toxicology and Applied Pharmacology 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 C7H8BClO2, Quality Control of 321673-30-7.

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

Serezani, Carlos H. published the artcileLeukotriene B₄ amplifies NF-κB activation in mouse macrophages by reducing SOCS1 inhibition of MyD88 expression, COA of Formula: C12H23N3S, the publication is Journal of Clinical Investigation (2011), 121(2), 671-682, database is CAplus and MEDLINE.

Activation of NF-κB and 5-lipoxygenase-mediated (5-LO-mediated) biosynthesis of the lipid mediator leukotriene B₄ (LTB₄) are pivotal components of host defense and inflammatory responses. However, the role of LTB₄ in mediating innate immune responses elicited by specific TLR ligands and cytokines is unknown. Here we have shown that responses dependent on MyD88 (an adaptor protein that mediates signaling through all of the known TLRs, except TLR3, as well as IL-1β and IL-18) are reduced in mice lacking either 5-LO or the LTB₄ receptor BTL1, and that macrophages from these mice are impaired in MyD88-dependent activation of NF-κB. This macrophage defect was associated with lower basal and inducible expression of MyD88 and reflected impaired activation of STAT1 and overexpression of the STAT1 inhibitor SOCS1. Expression of MyD88 and responsiveness to the TLR4 ligand LPS were decreased by Stat1 siRNA silencing in WT macrophages and restored by Socs1 siRNA in 5-LO-deficient macrophages. These results uncover a pivotal role in macrophages for the GPCR BLT1 in regulating activation of NF-κB through Stat1-dependent expression of MyD88.

Journal of Clinical Investigation 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 C26H31N3O3, COA of Formula: C12H23N3S.

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

Soni, Navneet Omprakash published the artcileTargeting LTB4 -BLT1 – in diabetic nephropathy?, Category: amides-buliding-blocks, the publication is World Journal of Pharmacy and Pharmaceutical Sciences (2017), 6(9), 312-315, database is CAplus.

A review. Lipid mediators play important role in renal injury many of lipid mediators are expressed and up regulated in response to toxins, drugs and in metabolic disorder. Lipid mediators also play role in vascular complication. So new intervention target can be thought by targeting the mediators Diabetic complication can be reduced unfortunately very few study are available to test the hypothesis and come to conclusion. But from all available study reports one can say targeting lipid mediators have future scope as well as limitation.

World Journal of Pharmacy and Pharmaceutical Sciences 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 C14H14, Category: amides-buliding-blocks.

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

Nobuaki, Miyahara published the artcileLTB4 and Allergies, Recommanded Product: [(2-Hexylcyclopentylidene)amino]thiourea, the publication is Arerugi, Men’eki (2018), 25(3), 362-370, database is CAplus.

A review. Mouth leukotriene B₄ (LTB₄) is a bioactive lipid derived from arachidonic acid. Since the identification of the high-affinity receptor BLT1 and the low-affinity receptor BLT2 of LTB₄, their involvement in various allergic diseases has been elucidated. LTB₄-BLT1 pathway has been suggested to be involved in bronchial apol., especially in severe acute infarct steroid-resistant apnea, and in atopic dermatitis, allergic rhinitis, conjunctivitis, etc : LTB₄-BLT1 regulation of the pathway is expected as a new bureaucracy for allergic diseases.

Arerugi, Men’eki 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

Gelfand, Erwin W. published the artcileImportance of the leukotriene B4-BLT1 and LTB4-BLT2 pathways in asthma, Recommanded Product: [(2-Hexylcyclopentylidene)amino]thiourea, the publication is Seminars in Immunology (2017), 44-51, database is CAplus and MEDLINE.

For several decades, the leukotriene pathways have been implicated as playing a central role in the pathophysiol. of asthma. The presence and elevation of numerous metabolites in the blood, sputum, and bronchoalveolar lavage fluid from asthmatics or exptl. animals adds support to this notion. However, targeting of the leukotriene pathways has had, in general, limited success. The single exception in asthma therapy has been targeting of the cysteinyl leukotriene receptor 1, which clin. has proven effective but only in certain clin. situations. Interference with 5-lipoxygenase has had limited success, in part due to adverse drug effects. The importance of the LTB4-BLT1 pathway in asthma pathogenesis has extensive exptl. support and findings, albeit limited, from clin. samples. The LTB4-BLT1 pathway was shown to be important as a neutrophil chemoattractant. Despite observations made more than two decades ago, the LTB4-BLT1 pathway has only recently been shown to exhibit important activities on subsets of T lymphocytes, both as a chemoattractant and on lymphocyte activation, as well as on dendritic cells, the major antigen presenting cell in the lung. The role of BLT2 in asthma remains unclear. Targeting of components of the LTB4-BLT1 pathway offers innovative therapeutic opportunities especially in patients with asthma that remain uncontrolled despite intensive corticosteroid treatment.

Seminars in 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, Recommanded Product: [(2-Hexylcyclopentylidene)amino]thiourea.

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

Feng, Yue-Hua published the artcileIncreased apolipoprotein M induced by lack of scavenger receptor BI is not activated via HDL-mediated cholesterol uptake in hepatocytes, Application of [(2-Hexylcyclopentylidene)amino]thiourea, the publication is Lipids in Health and Disease (2018), 200/1-200/8, database is CAplus and MEDLINE.

Background: Scavenger receptor BI (SR-BI) is a classic high-d. lipoprotein (HDL) receptor, which mediates selective lipid uptake from HDL cholesterol esters (HDL-C). Apolipoprotein M (ApoM), as a component of HDL particles, could influence preβ-HDL formation and cholesterol efflux. The aim of this study was to determine whether SR-BI deficiency influenced the expression of ApoM. Methods: Blood samples and liver tissues were collected from SR-BI gene knockout mice, and serum lipid parameters, including total cholesterol (TC), triglyceride (TG), high and low-d. lipoprotein cholesterol (HDL-C and LDL-C) and ApoM were measured. Hepatic ApoM and ApoAI mRNA levels were also determined In addition, BLT-1, an inhibitor of SR-BI, was added to HepG2 cells cultured with cholesterol and HDL, under serum or serum-free conditions. The mRNA and protein expression levels of ApoM were detected by RT-PCR and western blot. Results: We found that increased serum ApoM protein levels corresponded with high hepatic ApoM mRNA levels in both male and female SR-BI-/- mice. Besides, serum TC and HDL-C were also significantly increased. Treatment of HepG2 hepatoma cells with SR-BI specific inhibitor, BLT-1, could up-regulate ApoM expression in serum-containing medium but not in serum-free medium, even in the presence of HDL-C and cholesterol. Conclusions: Results suggested that SR-BI deficiency promoted ApoM expression, but the increased ApoM might be independent from HDL-mediated cholesterol uptake in hepatocytes.

Lipids in Health and Disease 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, Application of [(2-Hexylcyclopentylidene)amino]thiourea.

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

Sasaki, Fumiyuki published the artcileThe leukotriene receptors as therapeutic targets of inflammatory diseases, Recommanded Product: [(2-Hexylcyclopentylidene)amino]thiourea, the publication is International Immunology (2019), 31(9), 607-615, database is CAplus and MEDLINE.

A review. Leukotrienes (LTs) are inflammatory mediators derived from arachidonic acid. LTs include the di-hydroxy acid LT (LTB₄) and the cysteinyl LTs (CysLTs; LTC₄, LTD₄ and LTE₄), all of which are involved in both acute and chronic inflammation. We and other groups identified a high-affinity LTB₄ receptor, BLT1; the LTC₄ and LTD₄ receptors, CysLT1 and CysLT2; and the LTE₄ receptor, GPR99. Pharmacol. studies have shown that BLT1 signaling stimulates degranulation, chemotaxis and phagocytosis of neutrophils, whereas CysLT1 and CysLT2 signaling induces airway inflammation by increasing vascular permeability and the contraction of bronchial smooth muscle. Recently, we and other groups suggested that the LTB₄-BLT1 axis and the cysteinyl LTs-CysLT1/2 axis are involved in chronic inflammatory diseases including asthma, atopic dermatitis, psoriasis, atherosclerosis, arthritis, obesity, cancer and age-related macular degeneration using animal models for disease and gene knockout mice. This review describes the classical and novel functions of LTs and their receptors in several inflammatory diseases and discusses the potential clin. applications of antagonists for LT receptors and inhibitors of LT biosynthesis.

International 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, Recommanded Product: [(2-Hexylcyclopentylidene)amino]thiourea.

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