Meng Yan-Li, Wang Wei-Ming, Lv Dan-Dan, An Qiu-Xia, Lu Wei-Hong, Wang Xin, Tang Guixin
Heilongjiang Academy of Chinese Medicine Sciences, Harbin 150036, China.
Heilongjiang Academy of Chinese Medicine Sciences, Harbin 150036, China.
Environ Toxicol Pharmacol. 2017 Jan;49:188-193. doi: 10.1016/j.etap.2017.01.001. Epub 2017 Jan 3.
Platycodin D is one of the most important monomers of the Qinbaiqingfei pellet (Qinbai), which has already been approved as the first effective new Traditional Chinese Medicine used to fight against Mycoplasma pneumoniae (M. pneumoniae) in clinic in China. In previous studies, pharmacodynamics experiment has proved that Platycodin D has anti-M. pneumoniae effect and the minimum inhibitory concentration (MIC) is 16mμg/ml. This paper further clarified that the mechanism underlying the anti-M. pneumoniae effect of Platycodin D might be due to M. pneumoniae adhesion proteins P1 and P30. P1 and P30 expression levels in M. pneumoniae strain, M. pneumoniae-infected BALB/c mice, and M. pneumoniae-infected A549 cells were determined by reverse transcription PCR. Platycodin D strongly inhibited P1 and P30 expression in M. pneumonia and high dosage of Platycodin D exhibited a greater effect on reducing P1 and P30 expression than low dose Platycodin D. Platycodin D prevented M. pneumoniae infection through inhibiting the expression of adhesion proteins, which might be one of the mechanisms for the anti-M. pneumoniae properties of Qinbai. These results provide a foundation to further explore the mechanisms of action of Qinbai in future studies.
桔梗皂苷D是芩百清肺颗粒（芩百）最重要的单体之一，芩百已被批准为中国临床上首个用于对抗肺炎支原体的有效新型中药。在以往的研究中，药效学实验证明桔梗皂苷D具有抗肺炎支原体作用，最低抑菌浓度（MIC）为16μg/ml。本文进一步阐明，桔梗皂苷D抗肺炎支原体作用的机制可能与肺炎支原体黏附蛋白P1和P30有关。通过逆转录PCR测定肺炎支原体菌株、肺炎支原体感染的BALB/c小鼠及肺炎支原体感染的A549细胞中P1和P30的表达水平。桔梗皂苷D强烈抑制肺炎支原体中P1和P30的表达，高剂量桔梗皂苷D比低剂量桔梗皂苷D对降低P1和P30表达的作用更大。桔梗皂苷D通过抑制黏附蛋白的表达来预防肺炎支原体感染，这可能是芩百抗肺炎支原体特性的机制之一。这些结果为今后进一步探索芩百的作用机制提供了依据。
