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人参皂苷Rg3通过丝裂原活化蛋白激酶信号通路抑制肥大细胞介导的过敏性炎症。

Ginsenoside Rg3 suppresses mast cell-mediated allergic inflammation via mitogen-activated protein kinase signaling pathway.

作者信息

Kee Ji-Ye, Hong Seung-Heon

机构信息

Department of Oriental Pharmacy, College of Pharmacy, Wonkwang-Oriental Medicines Research Institute, Wonkwang University, Iksan, Jeonbuk, Republic of Korea.

出版信息

J Ginseng Res. 2019 Apr;43(2):282-290. doi: 10.1016/j.jgr.2018.02.008. Epub 2018 Mar 1.

Abstract

BACKGROUND

Ginsenoside Rg3 (G-Rg3) is the major bioactive ingredient of and has many pharmacological effects, including antiadipogenic, antiviral, and anticancer effects. However, the effect of G-Rg3 on mast cell-mediated allergic inflammation has not been investigated.

METHOD

The antiallergic effects of G-Rg3 on allergic inflammation were evaluated using the human and rat mast cell lines HMC-1 and RBL-2H3. Antiallergic effects of G-Rg3 were detected by measuring cyclic adenosine monophosphate (cAMP), detecting calcium influx, and using real-time reverse transcription polymerase chain reaction, enzyme-linked immunosorbent assay, Western blotting, and experiments.

RESULTS

G-Rg3 decreased histamine release from activated mast cells by enhancing cAMP levels and calcium influx. Proinflammatory cytokine production was suppressed by G-Rg3 treatment via regulation of the mitogen-activated protein kinases/nuclear factor-kappa B and receptor-interacting protein kinase 2 (RIP2)/caspase-1 signaling pathway in mast cells. Moreover, G-Rg3 protected mice against the IgE-mediated passive cutaneous anaphylaxis reaction and compound 48/80-induced anaphylactic shock.

CONCLUSION

G-Rg3 may serve as an alternative therapeutic agent for improving allergic inflammatory disorders.

摘要

背景

人参皂苷Rg3(G-Rg3)是[具体物质]的主要生物活性成分,具有多种药理作用,包括抗脂肪生成、抗病毒和抗癌作用。然而,G-Rg3对肥大细胞介导的过敏性炎症的影响尚未得到研究。

方法

使用人肥大细胞系HMC-1和大鼠肥大细胞系RBL-2H3评估G-Rg3对过敏性炎症的抗过敏作用。通过测量环磷酸腺苷(cAMP)、检测钙内流以及使用实时逆转录聚合酶链反应、酶联免疫吸附测定、蛋白质印迹和[具体实验名称]实验来检测G-Rg3的抗过敏作用。

结果

G-Rg3通过提高cAMP水平和钙内流减少活化肥大细胞中组胺的释放。G-Rg3处理通过调节肥大细胞中的丝裂原活化蛋白激酶/核因子-κB和受体相互作用蛋白激酶2(RIP2)/半胱天冬酶-1信号通路抑制促炎细胞因子的产生。此外,G-Rg3保护小鼠免受IgE介导的被动皮肤过敏反应和化合物48/80诱导的过敏性休克。

结论

G-Rg3可能作为一种改善过敏性炎症性疾病的替代治疗剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a33a/6437450/5b11296c43bb/gr1.jpg

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