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PM 2.5 and water-soluble components induce airway fibrosis through TGF-β1/Smad3 signaling pathway in asthmatic rats
Epidemiological studies have suggested that fine particulate matter (PM2.5) and asthma have been independently associated with pulmonary fibrosis but rarely studied together. Furthermore, it is unknown whether airway fibrosis in asthma is more attributable to water-soluble ions of PM2.5. Our current study was to explore the potential mechanism of PM2.5 and water-soluble components on airway fibrosis in ovalbumin (OVA)-sensitized asthmatic rats. Rats were intratracheally instilled with PM2.5 and water-soluble components every 3 days for 4 times or 8 times. Histopathological examination demonstrated that lung inflammatory and airway fibrosis were induced after PM2.5 and water-soluble components exposure. Meanwhile, PM2.5, in particular water-soluble extracts, increased expression of collagen 1 (COL-1), connective tissue growth factor (CTGF), interleukin-6 (IL-6), transforming growth factor-β1 (TGF-β1), Smad family member 3 (Smad3), and p-Smad3, whereas decreased secretion of heme oxygenase-1 (HO-1). However, pretreating asthmatic rats with SB432542, the inhibitor of TGF-β1, and SIS3 HCl, the antagonist of Smad3, both reversed the activation of airway fibrosis induced by water-soluble extracts. Therefore, TGF-β1/Smad3 signaling pathway may be responsible for the pathological process of airway fibrosis in asthmatic rats following PM2.5 and water-soluble components exposure.
Related Products
| Cat.No. | Product Name | Information |
|---|---|---|
| S7959 | SIS3 HCl | SIS3, a novel specific inhibitor of Smad3, inhibits TGF-β and activin signaling by suppressing Smad3 phosphorylation without affecting the MAPK/p38, ERK, or PI3-kinase signaling pathways. |
Related Targets
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