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蜂毒素和蜂毒肽对空气中真菌诱导的鼻息肉成纤维细胞化学介质和细胞外基质产生的影响。

The Effects of Melittin and Apamin on Airborne Fungi-Induced Chemical Mediator and Extracellular Matrix Production from Nasal Polyp Fibroblasts.

机构信息

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

Department of Pathology, School of Medicine, Catholic University of Daegu, Daegu 42472, Korea.

出版信息

Toxins (Basel). 2017 Oct 27;9(11):348. doi: 10.3390/toxins9110348.

DOI:10.3390/toxins9110348
PMID:29076987
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5705963/
Abstract

Melittin and apamin are the main components of bee venom and they have been known to have anti-inflammatory and anti-fibrotic properties. The aim of this study was to evaluate the effect of melittin and apamin on airborne fungi-induced chemical mediator and extracellular matrix (ECM) production in nasal fibroblasts. Primary nasal fibroblasts were isolated from nasal polyps, which were collected during endoscopic sinus surgery. Nasal fibroblasts were treated with and . The effects of melittin and apamin on the production of interleukin (IL)-6 and IL-8 were determined with enzyme linked immunosorbent assay. ECM mRNA and protein expressions were determined with the use of quantitative RT-PCR and Western blot. -induced IL-6 and IL-8 production was significantly inhibited by apamin. However, melittin did not influence the production of IL-6 and IL-8 from nasal fibroblasts. Melittin or apamin significantly inhibited collagen type I, TIMP-1, and MMP-9 mRNA expression and protein production from nasal fibroblasts. Melittin and apamin inhibited -induced phosphorylation of Smad 2/3 and p38 MAPK. Melittin and apamin can inhibit the fungi-induced production of chemical mediators and ECM from nasal fibroblasts. These results suggest the possible role of melittin and apamin in the treatment of fungi induced airway inflammatory diseases.

摘要

蜂毒肽和蜂毒素是蜜蜂毒液的主要成分，已被证明具有抗炎和抗纤维化特性。本研究旨在评估蜂毒肽和蜂毒素对空气中真菌诱导的鼻成纤维细胞化学介质和细胞外基质 (ECM) 产生的影响。从鼻息肉中分离出鼻成纤维细胞，这些息肉是在鼻内窥镜鼻窦手术中收集的。用 和 处理鼻成纤维细胞。通过酶联免疫吸附试验测定蜂毒肽和蜂毒素对白细胞介素 (IL)-6 和 IL-8 产生的影响。用定量 RT-PCR 和 Western blot 测定 ECM mRNA 和蛋白表达。蜂毒素显著抑制 诱导的 IL-6 和 IL-8 产生。然而，蜂毒肽并不影响鼻成纤维细胞中 IL-6 和 IL-8 的产生。蜂毒肽或蜂毒素显著抑制胶原 I、TIMP-1 和 MMP-9 mRNA 表达和鼻成纤维细胞的蛋白产生。蜂毒肽和蜂毒素抑制 诱导的 Smad 2/3 和 p38 MAPK 磷酸化。蜂毒肽和蜂毒素可抑制真菌诱导的鼻成纤维细胞产生化学介质和 ECM。这些结果表明蜂毒肽和蜂毒素可能在治疗真菌诱导的气道炎症性疾病中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fce/5705963/d20e86a0201a/toxins-09-00348-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fce/5705963/8759282c24e1/toxins-09-00348-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fce/5705963/20475a631317/toxins-09-00348-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fce/5705963/fe4d12aaa860/toxins-09-00348-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fce/5705963/1835c5278609/toxins-09-00348-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fce/5705963/d20e86a0201a/toxins-09-00348-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fce/5705963/8759282c24e1/toxins-09-00348-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fce/5705963/20475a631317/toxins-09-00348-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fce/5705963/fe4d12aaa860/toxins-09-00348-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fce/5705963/1835c5278609/toxins-09-00348-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fce/5705963/14877ba08eda/toxins-09-00348-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7fce/5705963/d20e86a0201a/toxins-09-00348-g006.jpg

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