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亚抑制浓度的prim-O-葡萄糖基升麻苷降低USA300中α-溶血素的表达。

Subinhibitory Concentrations of Prim-O-Glucosylcimifugin Decrease the Expression of Alpha-Hemolysin in (USA300).

作者信息

Ping Ouyang, Ruixue Yang, Jiaqiang Deng, Kaiyu Wang, Jing Fang, Yi Geng, Xiaoli Huang, Defang Chen, Weimin Lai, Li Tang, Lizi Yin

机构信息

College of Veterinary Medicine, Sichuan Agriculture University, Chengdu, China.

College of Animal Science and Technology, Sichuan Agriculture University, Chengdu, China.

出版信息

Evid Based Complement Alternat Med. 2018 Jul 19;2018:7579808. doi: 10.1155/2018/7579808. eCollection 2018.

DOI:10.1155/2018/7579808
PMID:30105064
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6076931/
Abstract

, an important opportunistic pathogen in human and animal, causes a series of diseases in the impairing of immunity of host and even then death. Alpha-hemolysin (Hla), a primary virulence factor, plays a major role in the pathogenic progress of , especially in pneumonia. Prim-O-glucosylcimifugin (POG), a nature chromone compound, is an active ingredient in many Chinese Medicines. In this study, POG investigated the inhibitory effect of the secretion of Hla in strain USA300 at the subinhibitory concentrations. The hemolysis assays and western blotting assays showed that POG can decrease the production of Hla in the USA300 growth cell cultures in a dose-dependent manner. The results of RT-PCR revealed that reduction of Hla was related to inhibit the transcription of and . In the cells experiment, POG was proved to protect A549 cells from Hla-medicated injury. In conclusion, POG was shown the capacity of decreased the production of Hla. POG can be developed as a candidate agent to treat infections against Hla.

摘要

作为人和动物体内一种重要的机会致病菌,在宿主免疫力受损时会引发一系列疾病,甚至导致死亡。α-溶血素(Hla)是主要的毒力因子,在其致病过程中起主要作用,尤其是在肺炎中。升麻素苷(POG)是一种天然色酮化合物,是多种中药中的活性成分。在本研究中,POG在亚抑菌浓度下研究了其对USA300菌株中Hla分泌的抑制作用。溶血试验和蛋白质印迹试验表明,POG能以剂量依赖的方式降低USA300生长细胞培养物中Hla的产生。RT-PCR结果显示,Hla的减少与抑制和的转录有关。在细胞实验中,POG被证明能保护A549细胞免受Hla介导的损伤。总之,POG显示出降低Hla产生的能力。POG可开发成为治疗针对Hla感染的候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a5a/6076931/20cf09173eee/ECAM2018-7579808.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a5a/6076931/e0f317f45650/ECAM2018-7579808.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a5a/6076931/9a034acd8924/ECAM2018-7579808.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a5a/6076931/5bd2c9c6165f/ECAM2018-7579808.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a5a/6076931/f80d4a738c4a/ECAM2018-7579808.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a5a/6076931/d6e75e9e943c/ECAM2018-7579808.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a5a/6076931/20cf09173eee/ECAM2018-7579808.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a5a/6076931/e0f317f45650/ECAM2018-7579808.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a5a/6076931/ce9bce3a8fc9/ECAM2018-7579808.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a5a/6076931/9a034acd8924/ECAM2018-7579808.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a5a/6076931/5bd2c9c6165f/ECAM2018-7579808.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a5a/6076931/f80d4a738c4a/ECAM2018-7579808.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a5a/6076931/d6e75e9e943c/ECAM2018-7579808.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8a5a/6076931/20cf09173eee/ECAM2018-7579808.007.jpg

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