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红参和 Rg3 对亚洲沙尘诱导的支气管上皮细胞 MUC5AC、MUC5B 和 MUC8 表达的影响。

Effect of Korean Red Ginseng and Rg3 on Asian Sand Dust-Induced MUC5AC, MUC5B, and MUC8 Expression in Bronchial Epithelial Cells.

机构信息

Department of Otolaryngology-Head and Neck Surgery, School of Medicine, Catholic University of Daegu, Daegu 42472, Korea.

出版信息

Molecules. 2021 Apr 1;26(7):2002. doi: 10.3390/molecules26072002.

DOI:10.3390/molecules26072002
PMID:33916022
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8037637/
Abstract

Korean Red ginseng (KRG), commonly used in traditional medicine, has anti-inflammatory, anti- oxidative, and anti-tumorigenic properties. Asian sand dust (ASD) is known to aggravate upper and lower airway inflammatory responses. BEAS-2B cells were exposed to ASD with or without KRG or ginsenoside Rg3. Mucin 5AC (MUC5AC), MUC5B, and MUC8 mRNA and protein expression levels were determined using quantitative RT-PCR and enzyme-linked immunosorbent assay. Nuclear factor kappa B (NF-κB), activator protein 1, and mitogen-activated protein kinase expression and activity were determined using western blot analysis. ASD induced MUC5AC, MUC5B, and MUC8 mRNA and protein expression in BEAS-2B cells, which was significantly inhibited by KRG and Rg3. Although ASD-induced mucin expression was associated with NF-κB and p38 mitogen-activated protein kinase (MAPK) activity, KRG and Rg3 significantly suppressed only ASD-induced NF-κB expression and activity. KRG and Rg3 inhibited ASD-induced mucin gene expression and protein production from bronchial epithelial cells. These results suggest that KRG and Rg3 have potential for treating mucus-producing airway inflammatory diseases.

摘要

高丽红参(KRG)在传统医学中被广泛应用,具有抗炎、抗氧化和抗肿瘤特性。已知亚洲沙尘(ASD)会加重上呼吸道和下呼吸道的炎症反应。本研究将 BEAS-2B 细胞暴露于含有或不含有 KRG 或人参皂苷 Rg3 的 ASD 中。通过定量 RT-PCR 和酶联免疫吸附试验测定粘蛋白 5AC(MUC5AC)、MUC5B 和 MUC8 mRNA 和蛋白表达水平。通过 Western blot 分析测定核因子 kappa B(NF-κB)、激活蛋白 1 和丝裂原活化蛋白激酶表达和活性。ASD 诱导 BEAS-2B 细胞中 MUC5AC、MUC5B 和 MUC8 mRNA 和蛋白表达,KRG 和 Rg3 显著抑制其表达。虽然 ASD 诱导的粘蛋白表达与 NF-κB 和 p38 丝裂原活化蛋白激酶(MAPK)活性有关,但 KRG 和 Rg3 仅显著抑制 ASD 诱导的 NF-κB 表达和活性。KRG 和 Rg3 抑制了支气管上皮细胞中 ASD 诱导的粘蛋白基因表达和蛋白产生。这些结果表明,KRG 和 Rg3 具有治疗粘液产生性气道炎症性疾病的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c925/8037637/0d7e02300d4a/molecules-26-02002-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c925/8037637/d49306251ee2/molecules-26-02002-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c925/8037637/15d2a5f3c74e/molecules-26-02002-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c925/8037637/0308371c4105/molecules-26-02002-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c925/8037637/770d3e73c702/molecules-26-02002-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c925/8037637/88afc8623512/molecules-26-02002-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c925/8037637/0d7e02300d4a/molecules-26-02002-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c925/8037637/d49306251ee2/molecules-26-02002-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c925/8037637/15d2a5f3c74e/molecules-26-02002-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c925/8037637/0308371c4105/molecules-26-02002-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c925/8037637/770d3e73c702/molecules-26-02002-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c925/8037637/88afc8623512/molecules-26-02002-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c925/8037637/0d7e02300d4a/molecules-26-02002-g006.jpg

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