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金叶番樱桃和红果仔HBK通过减少中性粒细胞黏附、脱颗粒和中性粒细胞胞外陷阱释放来抑制炎症反应。

Eugenia aurata and Eugenia punicifolia HBK inhibit inflammatory response by reducing neutrophil adhesion, degranulation and NET release.

作者信息

Costa Mírian Feliciano, Jesus Tais Iara, Lopes Bruno Rafael Pereira, Angolini Célio Fernando Figueiredo, Montagnolli Abner, Gomes Lorraine de Paula, Pereira Gabriela Sterle, Ruiz Ana Lucia Tasca Gois, Carvalho João Ernesto, Eberlin Marcos Nogueira, Dos Santos Catarina, Toledo Karina Alves

机构信息

Departamento de Ciências Biológicas, Faculdade de Ciências e Letras, Universidade Estadual Paulista -UNESP, Av Dom Antônio, 2100, Parque Universitário, ZIP 19806-900, Assis, SP, Brazil.

ThoMSon Laboratório de Espectrometria de Massas, Instituto de Química, Universidade Estadual de Campinas (UNICAMP), Campinas, 13083-970, Brazil.

出版信息

BMC Complement Altern Med. 2016 Oct 22;16(1):403. doi: 10.1186/s12906-016-1375-7.

DOI:10.1186/s12906-016-1375-7
PMID:27770779
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5075401/
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 of Eugenia aurata (EA) and Eugenia punicifolia HBK (EP) upon neutrophils.

METHODS

Ex vivo, isolated human neutrophils were sensitized by Eugenia 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 of Eugenia 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 of E. aurata and E. punicifolia HBK.

摘要

背景

番樱桃属植物在民间医学中用于治疗疼痛、糖尿病、肠道疾病和咳嗽。本研究的目的是在体外和体内评估金叶番樱桃(EA)和红果仔(EP)叶片的水乙醇提取物对中性粒细胞的抗炎活性。

方法

在体外,分离的人中性粒细胞用番樱桃属植物提取物(0.1 - 1000μg/mL)致敏,并用佛波酯刺激。在此条件下,测量与炎症过程相关的不同中性粒细胞活性:黏附、脱颗粒和中性粒细胞胞外陷阱释放。监测中性粒细胞活力和肿瘤细胞系。在体内,通过在预先用不同浓度番樱桃属植物提取物处理的小鼠中进行的腹膜炎模型评估中性粒细胞浸润。通过质谱法评估植物化学特征。

结果

在体外,EA和EP(1000μg/mL)分别降低了细胞黏附和脱颗粒。EA和EP均抑制中性粒细胞胞外陷阱释放。抗炎活性在无细胞毒性的情况下发生。在体内,EA和EP均抑制中性粒细胞迁移。植物化学特征显示,EA含有杨梅苷、芦丁、奎尼酸和槲皮素衍生物。EP含有没食子酸、槲皮素衍生物、丁香酸、鞣花酸、单没食子酰葡萄糖、糖基丁香酸、木丹苷B、六羟基联苯二甲酰葡萄糖异构体和双没食子酰葡萄糖异构体。EA和EP通过不同途径抑制中性粒细胞迁移。

结论

不同的化学成分可能解释了本文所述的EA和EP的抗炎作用。两种提取物均抑制中性粒细胞胞外陷阱释放,但只有EA降低细胞黏附,而EP减少弹性蛋白酶分泌。这项工作有助于阐明与金叶番樱桃和红果仔叶片抗炎活性相关的细胞机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1574/5075401/6abbf86b6dfb/12906_2016_1375_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1574/5075401/c69c26beae3e/12906_2016_1375_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1574/5075401/8aa6e6b8ac24/12906_2016_1375_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1574/5075401/6e0b6cd7642c/12906_2016_1375_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1574/5075401/d7684eefe42c/12906_2016_1375_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1574/5075401/6bc818848568/12906_2016_1375_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1574/5075401/6abbf86b6dfb/12906_2016_1375_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1574/5075401/c69c26beae3e/12906_2016_1375_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1574/5075401/8aa6e6b8ac24/12906_2016_1375_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1574/5075401/6e0b6cd7642c/12906_2016_1375_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1574/5075401/d7684eefe42c/12906_2016_1375_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1574/5075401/6bc818848568/12906_2016_1375_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1574/5075401/6abbf86b6dfb/12906_2016_1375_Fig6_HTML.jpg

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