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Baicalin Inhibits Airway Smooth Muscle Cells Proliferation through the RAS Signaling Pathway in Murine Asthmatic
Lingli Hu1,2,3, Lulu Li1,2, Chen Yan1,2
1Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, China.
Background:
Studies that looked at asthma airway remodeling pathogenesis and prevention have led to the discovery of the rat sarcoma viral oncogene (RAS) signaling pathway as a key mechanism that controls airway smooth muscle cell (ASMC) proliferation. Baicalin has great anti-inflammatory, proliferation-inhibited, and respiratory disease-relieving properties. However, the inhibitory effects and mechanisms of baicalin on ASMC-mediated airway remodeling in mice are still poorly understood.
Methods:
After establishing the asthmatic mice model by ovalbumin (OVA) and interfering with baicalin, airway remodeling characteristics such as airway resistance, mRNA, and protein expression levels of remodeling-related cytokines were measured by histopathological assessment, quantitative real-time polymerase chain reaction (qPCR), enzyme-linked immunosorbent assay (ELISA), and western blot. Further efforts on detailed mechanisms were used antibody arrays to compare the expression and activation of proteins involved in the RAS signaling pathway. In addition, validation experiments were performed in ASMC proliferation model and low-expression cells of the target gene by using shRNA.
Results:
In OVA-induced asthmatic mice model, baicalin significantly reduced the infiltration of inflammatory cells in lung tissue, attenuated airway resistance, and decreased mRNA and protein expression levels of remodeling-related cytokines such as interleukin-13 (IL-13), vascular endothelial growth factor (VEGF), transforming growth factor-beta 1 (TGF-β1), matrix metallopeptidase 9 (MMP9), and tissue inhibitor of metalloproteinase 1 (TIMP1). The results of antibody arrays involved in RAS signaling pathway revealed that OVA and baicalin administration altered the activation of protein kinase C alpha type (PKC-α), A-rapidly accelerated fibrosarcoma (A-RAF), mitogen-activated protein kinase 2 (MEK2), extracellular regulated MAP kinase (ERK), MAPK interacting serine/threonine kinase 1 (MNK1), and ETS transcription factor 1 (ELK1). The above results were further verified in the ASMC proliferation model. A-RAF silencing (shA-RAF) could promote ASMC proliferation and downregulate p-MEK2, p-ERK, p-MNK1, and p-ELK1 expression.
Conclusion:
The effects of baicalin against airway remodeling and ASMC proliferation might partially be achieved by suppressing the RAS signaling pathway. Baicalin may be a new therapeutic option for managing airway remodeling in asthma patients.
Insights
Baicalin effectively reduces airway remodeling in asthma by inhibiting airway smooth muscle cell proliferation. This study reveals baicalin
Area of Science:
- Pulmonology
- Pharmacology
- Cell Biology
Background:
- Asthma airway remodeling is linked to the rat sarcoma viral oncogene (RAS) signaling pathway controlling airway smooth muscle cell (ASMC) proliferation.
- Baicalin exhibits anti-inflammatory and proliferation-inhibiting properties relevant to respiratory diseases.
- The precise mechanisms of baicalin's effect on ASMC-mediated airway remodeling in mice remain unclear.
Purpose of the Study:
- To investigate the inhibitory effects of baicalin on airway remodeling in a mouse model of asthma.
- To elucidate the underlying mechanisms of baicalin's action, particularly its impact on the RAS signaling pathway.
- To assess baicalin's potential as a therapeutic agent for asthma-related airway remodeling.
Main Methods:
- Established an ovalbumin (OVA)-induced asthmatic mice model and treated with baicalin.
- Assessed airway remodeling using histopathology, measuring airway resistance, and quantifying cytokine expression (mRNA and protein) via qPCR and ELISA.
- Utilized antibody arrays to analyze RAS signaling pathway proteins and performed shRNA experiments for gene silencing validation in ASMCs.
Main Results:
- Baicalin significantly reduced inflammatory cell infiltration, attenuated airway resistance, and decreased key remodeling cytokines (IL-13, VEGF, TGF-β1, MMP9, TIMP1) in asthmatic mice.
- Baicalin modulated the activation of RAS pathway proteins including PKC-α, A-RAF, MEK2, ERK, MNK1, and ELK1.
- shRNA-mediated silencing of A-RAF promoted ASMC proliferation and downregulated downstream signaling molecules (p-MEK2, p-ERK, p-MNK1, p-ELK1).
Conclusions:
- Baicalin's anti-airway remodeling effects in asthma may involve the suppression of the RAS signaling pathway.
- Baicalin demonstrates potential as a novel therapeutic strategy for managing airway remodeling in asthma patients.
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