polymorphonuclear

L-Leucyl-L-Leucine methyl ester hydrochloride (Leu-Leu-ome hydrochloride) 是一种人单核细胞或多形核白细胞产生的 L-亮氨酸甲酯的二肽缩合产物。L-Leucyl-L-Leucine methyl ester hydrochloride 可选择性消除具有细胞毒性潜能的淋巴细胞，也可诱导溶酶体途径应激。

Gordonoside J是从菊花茎中分离出的化合物，抑制 LPS 诱导的大鼠多形核白细胞 （PMNS） 中一氧化氮的产生。

CJ-13,610 是一种具有口服活性的非氧化还原型 5-脂氧合酶 (5-LOX) 抑制剂。 CJ-13,610 抑制白三烯 B4 的生物合成并调节巨噬细胞中 IL-6 mRNA 的表达。

Traxanox 是一种可口服的利尿剂。Traxanox 在体外增强小鼠腹膜巨噬细胞或大鼠腹膜多形核白细胞对酵母颗粒的吞噬作用。Traxanox 对抑制BALB c小鼠抗体产生的恢复作用。

Traxanox TFA 是一种可口服的利尿剂。Traxanox TFA 在体外增强小鼠腹膜巨噬细胞或大鼠腹膜多形核白细胞对酵母颗粒的吞噬作用。Traxanox TFA 对抑制BALB c小鼠抗体产生的恢复作用。

Meclofenamate sodium is a potent non-steroidal anti-inflammatory agent, which can specifically inhibit chemokine-induced human polymorphonuclear leukocyte function: chemotaxis, degranulation, and superoxide anion free radical production.

(+)-Guaiacin is a compound isolated from the bark of Machilus wangchiana Chun. It shows potent in vitro activities against the release of β-glucuronidase in rat polymorphonuclear leukocytes (PMNs) induced by platelet-activating factor (PAF).

LY 178002 is an effective inhibitor of 5-lipoxygenase (5-LPO), phospholipase A2 (IC50: 0.6 μM for 5-lipoxygenase). LY 178002 also inhibits cellular production of LTB4 by human polymorphonuclear leukocytes and displays relatively weak inhibition on cycloox

D-Citrulline (H-D-Cit-OH)为L-citrulline的立体异构体。研究表明，D-Citrulline通过非NO介导机制，能有效减轻大鼠离体灌注心脏在缺血 再灌注条件下，由多形核白细胞 (PMN) 引发的心脏收缩功能障碍。

9-tert-Butyldoxycycline 具有免疫调节活性，它可改变多形核中性粒细胞的极化状态，并在缺血-再灌注损伤模型中改善炎症反应。此外，9-tert-Butyldoxycycline 是 Tet-On 转换系统的配体。

HZ52 是一种有效可逆的5-脂氧合酶(5-LO)抑制剂，在完整的人类多形核白细胞中可阻断白三烯的合成，IC50为 0.7 μM。

inhibits leukotriene B4 (LTB4)-induced polymorphonuclear neutrophils (PMN) chemotaxis

LY255283 是白三烯 B4 (LTB4) 受体的特异性拮抗剂，抑制人外周血多形核白细胞和由钙离子载体 A23187 激活的单核细胞中 LTB(4) 的产生。

L 651142 is a weak inhibitor of the platelet-activating factor receptor. It is also binding to polymorphonuclear leukocytes.

L 680833 is an orally active monocyclic beta-lactam human polymorphonuclear leukocyte elastase inhibitor.

Gea 3162 is a potent inhibitor of ADP-induced platelet aggregation in platelet rich plasma (PRP). GEA 3162 stimulates cGMP production in granulocytes, platelets, and polymorphonuclear leukocytes.

Traxanox sodium 是一种可口服的利尿剂。Traxanox sodium 在体外增强小鼠腹膜巨噬细胞或大鼠腹膜多形核白细胞对酵母颗粒的吞噬作用。Traxanox sodium 对抑制BALB c小鼠抗体产生的恢复作用。

PMX-205 is a cyclic hexapeptide that acts as a potent antagonist of C5a receptor (C5aR; IC50= 31 nM).1It is orally active and blocks inflammatory signaling and symptoms in animal models of colitis and allergic asthma.2,3PMX-205 is also brain penetrant and reduces neuroinflammation and neurodegeneration in an animal model of Alzheimer's disease.4 1.March, D.R., Proctor, L.M., Stoermer, M.J., et al.Potent cyclic antagonists of the complement C5a receptor on human polymorphonuclear leukocytes. Relationships between structures and activityMol. Pharmacol.65(4)868-879(2004) 2.Jain, U., Woodruff, T.M., and Stadnyk, A.W.The C5a receptor antagonist PMX205 ameliorates experimentally induced colitis associated with increased IL-4 and IL-10Br. J. Pharmacol.168(2)488-501(2013) 3.Staab, E.B., Sanderson, S.D., Wells, S.M., et al.Treatment with the C5a receptor/CD88 antagonist PMX205 reduces inflammation in a murine model of allergic asthmaInt. Immunopharmacol.21(2)293-300(2014) 4.Fonseca, M.I., Ager, R.R., Chu, S.-H., et al.Treatment with a C5aR antagonist decreases pathology and enhances behavioral performance in murine models of Alzheimer's diseaseJ. Immunol.183(2)1375-1383(2009)

Resolvin E2 (RvE2) is a member of the specialized pro-resolving mediator (SPM) family of bioactive lipids.1It is produced from eicosapentaenoic acidviaan 18-HEPE intermediate, which is formed by aspirin-acetylated COX-2-mediated oxidation of EPA, by 5-lipoxygenase (5-LO) in human polymorphonuclear (PMN) neutrophils.2,3RvE2 (20 ng/animal) inhibits increases in inflammatory exudate neutrophil infiltration in a mouse model of peritonitis induced by zymosan A .3Hepatic RvE2 levels are increased in mice fed normal chow, as well as in a mouse model of high-fat diet-induced non-alcoholic fatty liver disease (NAFLD), by dietary supplementation with EPA.4Plasma levels of RvE2 are increased by dietary supplementation with fish oil containing ω-3 polyunsaturated fatty acids (PUFAs) in patients with peripheral artery disease or chronic kidney disease.1,5,6 1.Chiang, N., and Serhan, C.N.Specialized pro-resolving mediator network: An update on production and actionsEssays Biochem.64(3)443-462(2020) 2.Tjonahen, E., Oh, S.F., Siegelman, J., et al.Resolvin E2: Identification and anti-inflammatory actions: Pivotal role of human 5-lipoxygenase in resolvin E series biosynthesisChemistry & Biology131193-1202(2006) 3.Sungwhan, F.O., Pillai, P.S., Recchiuti, A., et al.Pro-resolving actions and stereoselective biosynthesis of 18S E-series resolvins in human leukocytes and murine inflammationJ. Clin. Invest.121(2)569-581(2011) 4.Echeverría, F., Valenzuela, R., Espinosa, A., et al.Reduction of high-fat diet-induced liver proinflammatory state by eicosapentaenoic acid plus hydroxytyrosol supplementation: Involvement of resolvins RvE1/2 and RvD1/2J. Nutr. Biochem.6335-43(2019) 5.Ramirez, J.L., Gasper, W.J., Khetani, S.A., et al.Fish oil increases specialized pro-resolving lipid mediators in PAD (the OMEGA-PAD II trial)J. Surg. Res.238164-174(2019) 6.Barden, A.E., Shinde, S., Burke, V., et al.The effect of n-3 fatty acids and coenzyme Q10 supplementation on neutrophil leukotrienes, mediators of inflammation resolution and myeloperoxidase in chronic kidney diseaseProstaglandins Other Lipid Mediat.1361-8(2018)

Resolvins are a family of potent lipid mediators derived from both eicosapentaenoic acid and docosahexaenoic acid.[1] In addition to being anti-inflammatory, resolvins promote the resolution of the inflammatory response back to a non-inflamed state.[2] Resolvin D1 is produced physiologically from the sequential oxygenation of DHA by 15- and 5-lipoxygenase.[1] 17(R)-RvD1 is an aspirin-triggered epimer of RvD1 that reduces human polymorphonuclear leukocyte (PMN) transendothelial migration, the earliest event in acute inflammation, with equipotency to RvD1 (EC50 = ~30 nM).[3] 17(R)-RvD1 exhibits a dose-dependent reduction in leukocyte infiltration in a mouse model of peritonitis with maximal inhibition of ~35% at a 100 ng dose.[3] In contrast to RvD1, the aspirin-triggered form resists rapid inactivation by eicosanoid oxidoreductases. Analytical and biological comparisons of synthetic 17(R)-RvD1 with endogenously derived 17(R)-RvD1 have confirmed its identity as matching the natural product.[4]

17(R)-Protectin D1 is an aspirin-triggered epimer of the specialized pro-resolving mediator protectin D1 .1It decreases leukotriene B4-induced transendothelial migration of human polymorphonuclear (PMN) neutrophils when used at concentrations ranging from 0.1 to 10 nM. 17(R)-Protectin D1 (0.01-10 ng) reduces the recruitment of neutrophils in a mouse model of TNF-α-induced peritonitis. 1.Serhan, C.N., Fredman, G., Yang, R., et al.Novel proresolving aspirin-triggered DHA pathwayChem. Biol.18(18)976-987(2011)

Leukotriene B5 (LTB5) is a leukotriene with diverse biological activities. It is a metabolite of eicosapentaenoic acid formed through the 5-lipoxygenase (5-LO) pathway. LTB5 increases contraction of bullfrog lung strips ex vivo in a concentration-dependent manner. In vivo, LTB5 (100 nM) reduces tumor volume in mice injected with Tm1 murine melanoma cells. LTB5 also elicits chemokinesis and lysosomal enzyme release from polymorphonuclear leukocytes (PMNLs) 20- to 30-fold less, and induces platelet aggregation 8-fold less, potently than LTB4 .

C2 Phytoceramide is a bioactive semisynthetic sphingolipid that inhibits formyl peptide-induced oxidant release (IC50 = 0.38 μM) in suspended polymorphonuclear cells. It increases COX-2 protein levels 15-fold through ERK signaling. It induces death of keratinocytes (20% viability) with an ED50 value of 30 μM, the same concentration at which 35% of cells in a TUNEL assay are apoptotic. C2 Phytoceramide also has antiproliferative effects in CHO cells, with greater than 80% cytotoxicity achieved at a concentration of 20 μM, and induces internucleosomal DNA fragmentation. In addition, it inhibits the activation of phospholipase D (PLD) mediated by muscarinic acetylcholine receptors in vitro.

H-Leu-Leu-OMe . HBr 是由人单核细胞或多形核白细胞产生的L-亮氨酸甲酯的二肽缩合产物。 H-Leu-Leu-OMe . HBr 诱导内溶酶体途径应激并选择性地消除具有细胞毒性潜力的淋巴细胞。