Morusin alleviates mycoplasma pneumonia via the inhibition of Wnt/β-catenin and NF-κB signaling
Author(s) -
Cunrong Chen,
Jingjing Wang,
Jianfei Chen,
Lili Zhou,
Hui Wang,
Junnian Chen,
Zhihui Xu,
Shuaijun Zhu,
Wei Liu,
Ranjie Yu,
Junli Lu,
Haoteng Luo,
Min Chen,
Weiwen Chen
Publication year - 2019
Publication title -
bioscience reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.938
H-Index - 77
eISSN - 1573-4935
pISSN - 0144-8463
DOI - 10.1042/bsr20190190
Subject(s) - wnt signaling pathway , pneumonia , mycoplasma pneumoniae , tumor necrosis factor alpha , mycoplasma pneumonia , lung , interleukin , biology , microbiology and biotechnology , immunology , signal transduction , medicine , cytokine
Morusin has been traditionally used for the treatment of Mycoplasma pneumoniae pneumonia (MPP), but the underlying mechanism remains elusive. The present study aimed to explore the mechanism by which morusin achieves efficacy on mycoplasma pneumonia. Mycoplasma pneumonia model was established in BALB/c mouse and the effects of morusin were evaluated in the model. Compared with the model group, DNA amount of M. pneumoniae decreased by 24.6 ± 3.14% and 47.6 ± 6.78% in low morusin (20 mg/kg) and high morusin (50 mg/kg) groups, respectively ( P <0.05). Moreover, morusin treatment led to decreased levels of pro-inflammatory cytokines such as interleukin (IL)-6, IL-1β, and tumor necrosis factor α and increased level of anti-inflammatory IL-10 in mice lung tissue. Furthermore, morusin treatment inhibited the activation of Wnt/β-catenin and NF-κB pathways in mice lung tissue. Taken together, our results suggest that morusin relieves mycoplasma pneumonia via the inhibition of the activation of Wnt/β-catenin and NF-κB pathways, and is a potential natural agent for the treatment of mycoplasma pneumonia.
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