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紫苞姜提取物通过NF-κB和Akt/JNK信号通路减轻肿瘤坏死因子-α诱导的人内皮细胞血管黏附分子表达。

Etlingera pavieana extract attenuates TNF-α induced vascular adhesion molecule expression in human endothelial cells through NF-κB and Akt/JNK pathways.

作者信息

Srisook Klaokwan, Potiprasart Kamonporn, Sarapusit Songklod, Park Chang-Shin, Srisook Ekaruth

机构信息

Department of Biochemistry and Research Unit of Natural Bioactive Compounds for Healthcare Products Development, Faculty of Science, Burapha University, Chonburi, 20131, Thailand.

Center of Excellence for Innovation in Chemistry, Faculty of Science, Burapha University, Chonburi, Thailand.

出版信息

Inflammopharmacology. 2020 Dec;28(6):1649-1662. doi: 10.1007/s10787-019-00676-4. Epub 2019 Dec 12.

DOI:10.1007/s10787-019-00676-4
PMID:31832850
Abstract

The aim of this study was to determine whether ethanol extracts of Etlingera pavieana rhizomes (EPE) can inhibit the expression of ICAM-1 and VCAM-1 in TNF-α-stimulated human vascular endothelial cells. EPE significantly reduced ICAM-1 and VCAM-1 expression in a concentration-dependent manner. EPE also suppressed phospho-IκB level and nuclear translocation of NF-κB. EPE significantly inhibited phosphorylation of JNK and c-Jun, a major component of AP-1, but had no effects on ERK and p38 MAPK pathways. Akt phosphorylation was increased in the presence of EPE, and wortmannin and SP600125 reversed the inhibitory effects of EPE on ICAM-1 and VCAM-1 expression. Furthermore, the active EPE constituents 4-methoxycinnamyl p-coumarate and trans-4-methoxycinnamaldehyde attenuated TNF-α-induced expression of ICAM-1 and VCAM-1. Taken together, our data indicate that EPE protects against vascular inflammation in endothelial cells, in part via NF-κB and Akt/JNK signalings. In future studies, E. pavieana may be developed as a therapeutic agent or dietary supplement for treating and preventing inflammatory diseases.

摘要

本研究的目的是确定益智砂仁根茎乙醇提取物(EPE)是否能抑制肿瘤坏死因子-α(TNF-α)刺激的人血管内皮细胞中细胞间黏附分子-1(ICAM-1)和血管细胞黏附分子-1(VCAM-1)的表达。EPE以浓度依赖的方式显著降低了ICAM-1和VCAM-1的表达。EPE还抑制了磷酸化IκB水平和核因子-κB(NF-κB)的核转位。EPE显著抑制了应激活化蛋白激酶(JNK)和活化蛋白-1(AP-1)的主要成分c-Jun的磷酸化,但对细胞外信号调节激酶(ERK)和p38丝裂原活化蛋白激酶(MAPK)途径没有影响。在EPE存在的情况下,蛋白激酶B(Akt)的磷酸化增加,渥曼青霉素和SP600125可逆转EPE对ICAM-1和VCAM-1表达的抑制作用。此外,活性EPE成分4-甲氧基肉桂酰对香豆酸和反式-4-甲氧基肉桂醛减弱了TNF-α诱导的ICAM-1和VCAM-1的表达。综上所述,我们的数据表明,EPE可部分通过NF-κB和Akt/JNK信号通路保护内皮细胞免受血管炎症的影响。在未来的研究中,益智砂仁可能被开发成为一种治疗和预防炎症性疾病的治疗药物或膳食补充剂。

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