Eugenia aurata and Eugenia punicifolia HBK inhibit inflammatory response by reducing neutrophil adhesion, degranulation and NET release. Issue 1 (December 2016)

• Record Type: Journal Article
• Authors: Costa, Mírian; Jesus, Tais; Lopes, Bruno; Angolini, Célio; Montagnolli, Abner; Gomes, Lorraine; Pereira, Gabriela; Ruiz, Ana; Carvalho, João; Eberlin, Marcos; dos Santos, Catarina; Toledo, Karina
• Is Part Of: BMC complementary and alternative medicine. Volume 16:Issue 1(2016)
• Page Start: 1
• Page End: 10
• Publication Date: 2016-12
• Subjects: Inflammation -- Neutrophils -- Eugenia aurata -- Eugenia punicifolia (HBK) -- Adhesion -- Elastase; Alternative medicine -- Periodicals; Complementary Therapies -- Periodicals; 615.505
• DOI: 10.1186/s12906-016-1375-7
• Languages: English
• ISSNs: 1472-6882

Abstract

Abstract Background Eugenia spp. are used in popular medicine in the treatment of pain, diabetes, intestinal disorders and cough. The aim of the work is to evaluate, ex vivo and in vivo, the anti-inflammatory activity of the hydroethanolic extracts of the leaves ofEugenia aurata (EA) andEugenia punicifolia HBK (EP) upon neutrophils. Methods Ex vivo, isolated human neutrophils were sensitized byEugenia extracts (0.1–1000 μg/mL) and stimulated by PMA. In these conditions, different neutrophil activities related to inflammatory process were measured: adhesion, degranulation and NET release. Neutrophil viability and tumor line cells were monitored. In vivo, neutrophil influx was evaluated by peritonitis model performed in mice pretreated with different concentrations ofEugenia extracts. Phytochemical profile was assessed by mass spectrometry. Results Ex vivo, EA and EP (1000 μg/mL) reduced cell adhesion and degranulation, respectively. NET release was inhibited by EA and EP. Anti-inflammatory activities occurred in the absence of cytotoxicity. In vivo, both EA as EP inhibited neutrophil migration. The phytochemical profile revealed that EA contains myricitrin, rutin, quinic acid and quercetin derivatives. EP presents gallic acid, quercetin derivatives, syringic acid, ellagic acid, monogalloyl-glucose, glycosyringic acid, mudanoside B, HHDP glucose isomer and digalloylglucose isomer. EA and EP inhibit neutrophil migration by different pathways. Conclusion Different chemical compositions may explain the anti-inflammatory effects described herein for EA and EP. Both extracts inhibit NET release but only EA reduces cell adhesion whereas EP decreases elastase secretion. This work contributes to the elucidation of cellular mechanisms related to the anti-inflammatory activity for leaves ofE. aurata andE. punicifolia HBK.