Title:Mechanisms of Er Chen Tang on Treating Asthma Explored by Network
Pharmacology and Experimental Verification
Volume: 27
Issue: 2
Author(s): Yuzhe Ren, Haijing Zhang, Zhou Yu, Xiangzheng Yang and Deyou Jiang*
Affiliation:
- Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang, China
Keywords:
Er Chen Tang, pharmacology network, inflammation, TGF-β/STAT3 signaling pathway, ovalbumin, asthma.
Abstract:
Objective: The aim of this study is to explore the active ingredients of ECT and their
targets for asthma and investigate the potential mechanism of ECT on asthma.
Methods: Firstly, the active ingredients and target of ECT were screened for BATMAN and
TCMSP, and functional analysis was done via DAVID. Then, the animal model was induced by
ovalbumin (OVA) and aluminum hydroxide. Eosinophil (EOS) counts, EOS active substance Eosinophilic
cationic protein (ECP) and eotaxin levels were detected following the instruction. Pathological
changes in lung tissue were examined by H&E staining and transmission electron microscopy.
Interleukin (IL-4, IL-10, IL-13, TNF-α), TIgE and IgE levels in bronchoalveolar lavage fluid
(BALF) were measured by ELISA. Finally, the protein expression of the TGF-β / STAT3 pathway
to lung tissue was detected by Western Blot.
Results: A total of 450 compounds and 526 target genes were retrieved in Er Chen Tang. Functional
analysis indicated that its treatment of asthma was associated with inflammatory factors and
fibrosis. In the animal experiment, the results showed that ECT significantly regulated inflammatory
cytokine (IL-4, IL-10, IL-13, TNF-α) levels in (P<0.05, P<0.01, reduced EOS number (P<0.05)
and also ECP and Eotaxin levels in the blood (P<0.05) in BALF and/or plasma. Bronchial tissue
injury was obviously improved on ECT treatment. Associated proteins in TGF-β / STAT3 pathway
were significantly regulated by ECT (P<0.05).
Conclusion: This study originally provided evidence that the Er Chen Tang was effective in the
treatment of asthma symptoms, and its underlying mechanism might be the regulation of inflammatory
factor secretion and the TGF-β/STAT3 signaling pathway.