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积雪草苷通过抑制肥大细胞脱颗粒减轻变应性炎症。

Asiaticoside Mitigates the Allergic Inflammation by Abrogating the Degranulation of Mast Cells.

作者信息

Jiang Jing Zhi, Ye Jing, Jin Guang Yu, Piao Hong Mei, Cui Hong, Zheng Ming Yu, Yang Jin Shi, Che Nan, Choi Yun Ho, Li Liang Chang, Yan Guang Hai

机构信息

Department of Anatomy, Histology and Embryology, Medical College of Yanbian University , Yanji 133002, Jilin, China.

Department of Respiratory Medicine, Yanbian University Hospital , Yanji 133000, Jilin China.

出版信息

J Agric Food Chem. 2017 Sep 20;65(37):8128-8135. doi: 10.1021/acs.jafc.7b01590. Epub 2017 Sep 11.

DOI:10.1021/acs.jafc.7b01590
PMID:28891650
Abstract

The effects of asiaticoside (AS) on allergic responses mediated by mast cells were investigated. AS showed no obvious cytotoxicity on RPMCs (rat peritoneal mast cells). AS reduced the intracellular calcium in RPMCs and deprived the histamine release and degranulation. AS also decreased the generation of antigen-induced tumor necrosis factor α, interleukin (IL)-4, IL-8, and IL-1β in RBL-2H3 cells sensitized by IgE. The suppression of AS on pro-inflammatory cytokines was related with the activation of the intracellular FcεRI and the inhibition of the nuclear factor-κB signaling pathway. In addition, AS disabled the phosphorylation of antigen-induced Syk, Lyn, Gab2, and PLCγ1, thus suppressing the downstream Akt phosphorylation and MAPKs pathways. It also increased HO-1 and Nrf2 expression time dependently. In summary, we demonstrate that AS suppresses the allergic inflammation mediated by mast cells and this effect might be mediated by FcεRI-dependent signaling pathways.

摘要

研究了积雪草苷(AS)对肥大细胞介导的过敏反应的影响。AS对大鼠腹膜肥大细胞(RPMCs)无明显细胞毒性。AS降低了RPMCs内的钙离子浓度,抑制了组胺释放和脱颗粒。AS还减少了IgE致敏的RBL-2H3细胞中抗原诱导的肿瘤坏死因子α、白细胞介素(IL)-4、IL-8和IL-1β的产生。AS对促炎细胞因子的抑制作用与细胞内FcεRI的激活及核因子κB信号通路的抑制有关。此外,AS抑制了抗原诱导的Syk、Lyn、Gab2和PLCγ1的磷酸化,从而抑制了下游的Akt磷酸化和丝裂原活化蛋白激酶(MAPKs)通路。AS还能时间依赖性地增加血红素加氧酶-1(HO-1)和核因子E2相关因子2(Nrf2)的表达。总之,我们证明AS可抑制肥大细胞介导的过敏性炎症,且这种作用可能是由FcεRI依赖性信号通路介导的。

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