Bueno-Silva Bruno, Bueno Manuela Rocha, Kawamoto Dione, Casarin Renato C, Pingueiro João Marcos Spessoto, Alencar Severino Matias, Rosalen Pedro Luiz, Mayer Marcia Pinto Alves
Department of Microbiology, Institute of Biomedical Sciences, University of São Paulo, São Paulo 05508-900, SP, Brazil.
Dental Research Division, Guarulhos University, Guarulhos 07023-070, SP, Brazil.
Pharmaceuticals (Basel). 2022 Apr 29;15(5):553. doi: 10.3390/ph15050553.
The isoflavone (3)-vestitol, obtained from red propolis, has exhibited anti-inflammatory, antimicrobial, and anti-caries activity; however, few manuscripts deal with its anti-inflammatory mechanisms in macrophages. The objective is to elucidate the anti-inflammatory mechanisms of (3)-vestitol on those cells. Peritoneal macrophages of C57BL6 mice, stimulated with lipopolysaccharide, were treated with 0.37 to 0.59 µM of (3)-vestitol for 48 h. Then, nitric oxide (NO) quantities, macrophages viability, the release of 20 cytokines and the transcription of several genes related to cytokine production and inflammatory response were evaluated. The Tukey-Kramer variance analysis test statistically analyzed the data. (3)-vestitol 0.55 µM (V55) lowered NO release by 60% without altering cell viability and diminished IL-1β, IL-1α, G-CSF, IL-10 and GM-CSF levels. V55 reduced expression of , and (associated to inflammation and tissue destruction in periodontitis) and , , (correlated to atherosclerosis). V55 increased expression of and genes (inhibitors of cytokine signaling and NF-κB pathway), (associated to atherosclerosis control), (encoder a protein with analogous effects to insulin) and (fibroblasts growth factor). (3)-vestitol anti-inflammatory mechanisms involve cytokines and NF-κB pathway inhibition. Moreover, (3)-vestitol may be a candidate for future in vivo investigations about the treatment/prevention of persistent inflammatory diseases such as atherosclerosis and periodontitis.
从红蜂胶中提取的异黄酮（3）-vestitol已表现出抗炎、抗菌和抗龋活性；然而，很少有手稿涉及它在巨噬细胞中的抗炎机制。目的是阐明（3）-vestitol对这些细胞的抗炎机制。用脂多糖刺激C57BL6小鼠的腹腔巨噬细胞，并用0.37至0.59μM的（3）-vestitol处理48小时。然后，评估一氧化氮（NO）量、巨噬细胞活力、20种细胞因子的释放以及与细胞因子产生和炎症反应相关的几个基因的转录。Tukey-Kramer方差分析测试对数据进行统计学分析。0.55μM的（3）-vestitol（V55）使NO释放降低60%，而不改变细胞活力，并降低IL-1β、IL-1α、G-CSF、IL-10和GM-CSF水平。V55降低了（与牙周炎中的炎症和组织破坏相关）以及（与动脉粥样硬化相关）的表达。V55增加了基因（细胞因子信号传导和NF-κB途径的抑制剂）、（与动脉粥样硬化控制相关）、（编码一种具有类似胰岛素作用的蛋白质）和（成纤维细胞生长因子）的表达。（3）-vestitol的抗炎机制涉及细胞因子和NF-κB途径的抑制。此外，（3）-vestitol可能是未来关于治疗/预防动脉粥样硬化和牙周炎等持续性炎症疾病的体内研究的候选药物。
