peritonitis

Dicloxacillin Sodium hydrate 是一种青霉素类窄谱β内酰胺抗生素，可研究革兰氏阳性菌感染。

BMS-813160 是CCR2/CCR5双重拮抗剂。有用于心血管的研究潜力。

GS-441524 是 Remdesivir 的主要活性代谢物，活性更优于 Remdesivir ，治疗患有自然发生的猫传染性腹膜炎的猫。

Cloxacillin sodium monohydrate (Cloxacillin Sodium) 有抗菌作用，对Staphylococcus aureus25923 的最小抑菌浓度为256 mg/L。

AA 2379 是一种可口服的抗风湿剂，有抗炎和解热活性，剂量依赖性地抑制由补体介导的大鼠酵母聚糖诱导的爪水肿和小鼠酵母聚糖活化血清诱导的腹膜炎。

Sodium Thioglycolate是一种针对二硫化物的强还原剂，能够分解毛发中的角蛋白，能够构建腹膜炎动物模型，可用于生物化学实验和药物合成研究。

NDM-1 inhibitor-7 (Compound A8) 是一种IC50为10.284 μM的NDM-1抑制剂。它能够恢复MEM穿透革兰氏阴性菌细胞壁的能力，并有效恢复MEM对NDM-1阳性大肠杆菌的抗菌功效。在Galleria mellonella感染模型和鼠腹膜炎感染模型中，NDM-1 inhibitor-7表现出显著疗效。

NLRP3-IN-75 是一种能够有效口服的NLRP3抑制剂。该化合物能以IC50为23 nM的浓度抑制IL-1β的分泌，选择性地通过破坏炎症小体的组装抑制NLRP3的活化，同时不影响NLRC4或AIM2炎症小体的组装。NLRP3-IN-75 在急性腹膜炎、糖尿病肾病和炎症性肠病 (IBD) 等模型中展现出显著的抗炎作用。

AS-605240 (potassium) 是一种可口服的PI3Kγ抑制剂 (IC50: 8 nM; Ki: 7.8 nM)。该化合物能够抑制 MCP-1 和 CSF1 诱导的 PKB 磷酸化 (IC50分别为 0.181 和 0.550 µM)。在 RANTES (CCL5) 和巯基乙酸盐诱导的腹膜炎小鼠模型中，AS-605240 (potassium) 可以减少中性粒细胞的募集 (EC50分别为 9.1 和 10 mg/kg)。此外，AS-605240 (potassium) 对 αCII-IA 诱发的小鼠关节炎有改善作用。

NLRP3-IN-79 (Compound B6) 是一种选择性NLRP3 inflammasome抑制剂，其IC50为10.69 nM。它通过干扰NEK7-NLRP3的相互作用来阻止NLRP3炎性体的组装。NLRP3-IN-79 可能在系统性炎症、腹膜炎和结肠炎等NLRP3驱动的炎症性疾病研究中具有应用潜力。

HDAC6-IN-54 (Compound 9m) 是一种具有高选择性的HDAC6（组蛋白去乙酰化酶 6）抑制剂，其IC50值为0.021 μM。HDAC6-IN-54 能有效阻断NLRP3炎性小体的激活，缓解与NLRP3炎性小体相关的疾病症状，如急性腹膜炎、炎症性肠病及银屑病等。

ZY39 是一种选择性酪蛋白水解蛋白酶 P（ClpP）激动剂，通过选择性激活金黄色葡萄球菌 ClpP（SaClpP）来抑制多重耐药菌株的生长。ZY39 在体外也能促进人源 ClpP（HsClpP）的酶促水解。ZY39 在金黄色葡萄球菌感染的小鼠腹膜炎模型中抑制多重耐药菌株生长。ZY39 可用于金黄色葡萄球菌感染的相关研究。

MAO-A/B-IN-4 是一种口服活性的 MAO-A/B 抑制剂，其 IC50 值分别为 51.3 μM 和 47.0 μM。MAO-A/B-IN-4 对 S. aureus、MSSA、MRSA、LRSA 和 LREFa 展现出强效活性，并在小鼠 LRSA 腹膜炎感染模型中具有显著的抗菌功效。该化合物可用于细菌感染研究。

NPSR1 antagonist-1 是一种有效且具有外周限制性的神经肽 S 受体 1 (NPSR1) 拮抗剂。它能够抑制 IL-6、PTGS2、IL-20 和 CXCL8 的表达，并降低 TNF-α 细胞因子水平。此化合物可用于腹膜炎等炎症相关研究。

NLRP3-IN-84 (Compound 32) 是一种NLRP3炎症小体抑制剂，它通过抑制NLRP3 ATP酶 (NLRP3 ATPase) 的活性（IC50= 158.4 nM），干扰NLRP3的寡聚化。此外，NLRP3-IN-84 抑制Caspase-1（IC50= 27.7 nM）、IL-1β的释放（PBMC：IC50= 19.5 nM；mPBMC：IC50= 24.2 nM）以及ASC斑点的形成（IC50= 131 nM）。该化合物对NLRC4和AIM2炎症小体无抑制活性，并且在小鼠急性腹膜炎模型中表现出显著的体内抗炎效果。NLRP3-IN-84 可用于研究与NLRP3相关的炎症性疾病。

CAI0019 是一种口服有效的 α-碳酸酐酶 (α-carbonic anhydrase) 抑制剂，基于Acetazolamide的骨架。其对肠球菌表现出窄谱抗菌活性，MIC50为 0.094 μM，MIC90为 0.39 μM。在败血性腹膜炎小鼠模型中，CAI0019 选择性抑制肠球菌，对大多数肠道共生菌未产生影响。

Benzo-17R-RvD2 是 RvD2 的含苯并类似物。它能增强人巨噬细胞的吞噬功能，限制中性粒细胞的浸润，降低 TNF-α 水平，并提高腹膜炎中 IL-1 受体拮抗剂的活性。此外，Benzo-17R-RvD2 促进人白细胞杀灭大肠杆菌，减少中性粒细胞的聚集面积，而不影响其抗念珠菌的活性。Benzo-17R-RvD2 能激活人 RvD2 受体，其 EC50 值约为 1.5 nM。该化合物可用于炎症相关疾病的研究，包括心血管疾病、癌症、神经炎症、疼痛和肌肉再生。

sEH/FLAP-IN-2 是一种具选择性的sEH (IC50= 12.6 nM) 和 FLAP 的双重抑制剂，可有效降低 5-LOX/FLAP 和 sEH 衍生的脂质体水平，从而促进脂质体的再分布。sEH/FLAP-IN-2 可用于腹膜炎相关研究。

A-987306 是一种高效、口服生物可利用的组胺H4拮抗剂，对大鼠和人 H4作用的Ki 值分别为 3.4 nM 和 5.8 nM。 A-987306 在小鼠腹膜炎模型中显示出抗炎活性。

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)

Resolvin conjugate in tissue regeneration 1 (RCTR1) is a specialized pro-resolving mediator (SPM) biosynthesized from docosahexaenoic acid by isolated human macrophages and apoptotic polymorphonuclear (PMN) neutrophils.1It has been found in human spleen and bone marrow.2RCTR1 is produced via lipoxygenase-mediated oxidation of DHA to 7(S)-8-epoxy-17(S)-HDHA, which is conjugated to glutathione.1,2,3RCTR1 (10 nM) increases phagocytosis ofE. colior apoptotic neutrophils in isolated human monocyte-derived macrophages.2It decreases chemotaxis induced by leukotriene B4in isolated human neutrophils when used at a concentration of 10 nM. RCTR1 (1 and 10 nM) accelerates tissue regeneration in planaria. Intraperitoneal administration of RCTR1 (100 ng/animal) shortens the inflammatory resolution period and decreases inflammatory exudate neutrophil infiltration in a mouse model ofE. coli-induced peritonitis. 1.Dalli, J., Ramon, S., Norris, P.C., et al.Novel proresolving and tissue-regenerative resolvin and protectin sulfido-conjugated pathwaysFASEB J.29(5)2120-2136(2015) 2.de la Rosa, X., Norris, P.C., Chiang, N., et al.Identification and complete stereochemical assignments of the new resolvin conjugates in tissue regeneration in human tissues that stimulate proresolving phagocyte functions and tissue regenerationAm. J. Pathol.188(4)950-966(2018) 3.Rodriguez, A.R., and Spur, B.W.First total synthesis of pro-resolving and tissue-regenerative resolvin sulfido-conjugatesTetrahedron Lett.58(16)1662-1668(2017)

Protectin conjugates in tissue regeneration 1 (PCTR1) is a specialized pro-resolving mediator (SPM) synthesized from docosahexaenoic acid . DHA is oxidized to 16S,17S-epoxy-protectin, which is then converted to PCTR1 by glutathione S-transferase. PCTR1 levels increase during resolution of acute microbial-induced peritonitis in mice. PCTR1 (30 ng, i.p.) administration 12 hours post-infection increases macrophage numbers and activity and shortens the resolution phase of inflammation by 57%. It also reduces the levels of PGE2 , PGD2 , and TXB2 in peritoneal exudates.