Modulation of P1 and EGF expression by Baicalin

Mycoplasma pneumoniae (M. pneumoniae) is increasingly recognized as a major cause of acute respiratory tract infections. Today, macrolides are used in the primary treatment of M. pneumoniae infection. However, with the increasing prevalence of strains resistant to macrolides, as well as reports of t...

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Bibliographic Details
Published in:International journal of molecular sciences 2012-12, Vol.14 (1), p.146-157
Main Authors: Meng, Yanli, Huo, Jinhai, Lu, Weihong, Wang, Xin, Zhang, Junwei, Wang, Weiming
Format: Article
Language:English
Subjects:
Adhesins, Bacterial - genetics
Adhesins, Bacterial - metabolism
Animals
Baicalin
Cell division
Chinese medicine
Drug resistance
EGF
EGF Family of Proteins - genetics
EGF Family of Proteins - metabolism
Epidermal growth factor
Flavonoids - pharmacology
Fluorescent Antibody Technique
Gene Expression Regulation - drug effects
Humans
Infections
Lung - drug effects
Lung - pathology
M. pneumoniae
Mice, Inbred BALB C
Motility
Mycoplasma pneumoniae - drug effects
Mycoplasma pneumoniae - genetics
Pneumonia
Proteins
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - genetics
RNA, Messenger - metabolism
Toxicity
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Summary:Mycoplasma pneumoniae (M. pneumoniae) is increasingly recognized as a major cause of acute respiratory tract infections. Today, macrolides are used in the primary treatment of M. pneumoniae infection. However, with the increasing prevalence of strains resistant to macrolides, as well as reports of toxicity and adverse side effects, it is necessary to develop an alternative therapeutic agent. A compound recipe - Qinbaiqingfei pellets (Qinbai) - have already been approved in China as the first effective traditional Chinese medicine to be used against M. pneumoniae. Herein, we characterize the mechanism by which Qinbai interacts with M. pneumoniae and lung epithelial cells. The fact that Baicalin is the key component of Qingbai leads us to believe its study is important to elucidating the mechanism of the action of Qinbai. In this study, we describe the complex impact of Baicalin on the adhesin protein P1 of M. pneumoniae and on the expression of epidermal growth factor (EGF) in BALB/c mice and A549 cells infected with M. pneumonia. We draw the conclusion that Baicalin not only cured M. pneumoniae infection by inhibiting P1 expression, but also enhanced the repair of lung epithelial cells by upregulating EGF. Finally, we demonstrate that Baicalin plays a role in Qinbai treatment.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms14010146