Abstract：
OBJECTIVE: This study aims to investigate the anti-inflammatory mechanism of monoamine oxidase inhibitor (MAOI) in carrageenan (CARR) induced inflammation models to reprofile their use. We also aimed to explore the role of monoamine oxidase (MAO)-mediated H2O2-NF-κB-COX-2 pathway in acute inflammation.
METHODS: In vitro anti-inflammatory activity and hydrogen peroxide (H2O2) scavenging activity were performed according to the established procedure. Inflammation was induced using CARR in BALB/c mice at the foot paw and peritoneal cavity. Hourly measurement of paw swelling was performed. The level of nitric oxide (NO), myeloperoxidase (MPO), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2) and nuclear factor κB (NF-κB) was determined using enzyme-linked immunosorbent assay (ELISA). Peritoneal fluid was collected to investigate total count, differential count of leukocytes, and capillary permeability.
RESULTS: In vitro anti-inflammatory evaluations revealed the potential role of MAOI to inhibit heat-induced protein denaturation and human red cell membrane destabilization. H2O2 inhibition activity of MAOI also proved their powerful role as an H2O2 scavenger. Treatment with MAOI in CARR-induced mice significantly reduced paw edema, leukocyte extravasation, and total and differential leukocyte count. The result of ELISA showed MAOI effectively reduce the level of COX-2, PGE2 and NF-κB in inflamed tissue.
CONCLUSIONS: In short, this study demonstrates that inhibition of H2O2 by MAOI alleviates CARR-induced paw edema possibly by inhibiting the H2O2-mediated NF-κB-COX-2 pathway. The present investigation identifies MAOI might reprofile for the treatment of acute inflammation also, the MAO enzyme may use as a novel therapeutic target to design and develop new class of anti-inflammatory agents.
METHODS: In vitro anti-inflammatory activity and hydrogen peroxide (H2O2) scavenging activity were performed according to the established procedure. Inflammation was induced using CARR in BALB/c mice at the foot paw and peritoneal cavity. Hourly measurement of paw swelling was performed. The level of nitric oxide (NO), myeloperoxidase (MPO), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2) and nuclear factor κB (NF-κB) was determined using enzyme-linked immunosorbent assay (ELISA). Peritoneal fluid was collected to investigate total count, differential count of leukocytes, and capillary permeability.
RESULTS: In vitro anti-inflammatory evaluations revealed the potential role of MAOI to inhibit heat-induced protein denaturation and human red cell membrane destabilization. H2O2 inhibition activity of MAOI also proved their powerful role as an H2O2 scavenger. Treatment with MAOI in CARR-induced mice significantly reduced paw edema, leukocyte extravasation, and total and differential leukocyte count. The result of ELISA showed MAOI effectively reduce the level of COX-2, PGE2 and NF-κB in inflamed tissue.
CONCLUSIONS: In short, this study demonstrates that inhibition of H2O2 by MAOI alleviates CARR-induced paw edema possibly by inhibiting the H2O2-mediated NF-κB-COX-2 pathway. The present investigation identifies MAOI might reprofile for the treatment of acute inflammation also, the MAO enzyme may use as a novel therapeutic target to design and develop new class of anti-inflammatory agents.
摘要：
目的：本研究旨在探讨单胺氧化酶抑制剂（MAOI）在角叉菜胶（CARR）诱导的炎症模型中的抗炎机制，以重新描述其用途。我们还旨在探讨单胺氧化酶（MAO）介导的H2O2-NF-κB-COX-2通路在急性炎症中的作用。
方法：根据已建立的程序进行体外抗炎活性和过氧化氢（H2O2）清除活性。在BALB/c小鼠的足爪和腹膜腔使用CARR诱导炎症。进行爪膨胀的每小时测量。一氧化氮（NO）的水平，髓过氧化物酶(MPO),环氧合酶-2（COX-2），采用酶联免疫吸附试验（ELISA）测定前列腺素E2（PGE2）和核因子κB（NF-κB）。收集腹膜液以调查总计数，白细胞分类计数，和毛细管通透性。
结果：体外抗炎评估揭示了MAOI抑制热诱导的蛋白质变性和人红细胞膜不稳定的潜在作用。MAOI的H2O2抑制活性也证明了其作为H2O2清除剂的强大作用。在CARR诱导的小鼠中使用MAOI治疗可显着减少爪水肿，白细胞外渗,白细胞总数和分类计数。ELISA结果显示MAOI能有效降低炎症组织中COX-2、PGE2和NF-κB的水平。
结论：简而言之，这项研究表明，MAOI对H2O2的抑制作用可能通过抑制H2O2介导的NF-κB-COX-2通路来减轻CARR引起的爪水肿。目前的调查发现MAOI也可能对急性炎症的治疗进行重新描述，MAO酶可作为一种新的治疗靶点来设计和开发新类抗炎药。
方法：根据已建立的程序进行体外抗炎活性和过氧化氢（H2O2）清除活性。
结果：体外抗炎评估揭示了MAOI抑制热诱导的蛋白质变性和人红细胞膜不稳定的潜在作用。
结论：简而言之，
