阿尔特米西宁可以通过抑制其叶发育来抑制由Candida albicans引起的口腔候群病
Xiaoyue Liang1, Ding Chen1, Jiannan Wang1
1State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases & West China Hospital of Stomatology, Sichuan University, Chengdu, China.
International journal of oral science
|September 12, 2023
概括
包括arteether在内的7种artemisinins有效地抑制了Candida albicans的状细胞发育,这是一个关键的毒性因素. 这种抗病毒性策略显示出治疗口腔候群病的前景,即使是耐药菌株.
科学领域:
- 菌类学 菌类学是指菌类学.
- 传染性疾病 传染性疾病
- 药理学 药理学是指药理学的学科.
背景情况:
- 香虫 (Candida albicans) 是口腔香病的主要原因.
- 抗真菌耐药性和副作用需要新的治疗策略.
- 抗病毒方法为直接杀死病原体提供了一个有希望的替代方案.
研究的目的:
- 为了研究七种阿尔特米西宁对Candida albicans的疗效.
- 探索阿尔特米西宁作为治疗口腔候群病的抗病毒性潜力.
- 阐明阿尔特米西宁抗菌活性背后的分子机制.
主要方法:
- 七种阿尔特米西宁被测试了它们对Candida albicans生长和状细胞发育的影响.
- 进行了转录组分析,以了解arteether的分子标.
- 进行了ATP和cAMP生产测定,以及Ras1过度表达菌株实验.
- 活体内疗效和毒性在小鼠口腔喉候群病模型中进行了评估.
主要成果:
- 阿尔特米西宁显著抑制了Candida albicans的状细胞发育,而不会影响真菌生长.
- 阿尔特以太表现出最强的抑制活性,对状细胞的形成和减少上皮细胞损伤.
- 发现阿尔特米西宁可以抑制ATP和cAMP的产生,调节Ras1-cAMP-Efg1通路.
- 在无系统毒性的情况下,Arteether在活体中有效地降低了对可纳敏感和耐药菌株的真菌负担.
结论:
- 艺术素,特别是艺术,是Candida albicans的有效抑制剂.
- 这项研究确定了artemisinins作为治疗口腔候群病的潜在抗病毒剂.
- 向叶发育是对抗耐药Candida albicans感染的可行策略.
相关概念视频
01:19Oral Hypoglycemic Agents: α-Glucosidase Inhibitors
203
α-glucosidase inhibitors, including acarbose (Precose), miglitol (Glyset), and voglibose (Voglib) (primarily available in Asia), are drugs that control blood sugar levels by delaying the digestion of starch and disaccharides. They achieve this by inhibiting α-glucosidase enzymes in the intestine, which slow the absorption of carbohydrates in the intestine, which in turn leads to a prolonged release of the glucoregulatory hormone GLP-1 from intestinal L-cells.
Acarbose and miglitol are...
Acarbose and miglitol are...
203
01:28Gene Regulation in Microbial Communities: Quorum Sensing
38
Quorum sensing is a mechanism of bacterial communication that enables coordinated gene expression in response to changes in population density. This facilitates collective behaviors that enhance survival, resource acquisition, and ecological adaptation. This process relies on small signaling molecules called autoinducers that accumulate as bacterial populations grow. When a critical threshold concentration of autoinducers is reached, bacterial cells collectively modify gene expression,...
38