Baicalin alleviates silica-induced lung inflammation and fibrosis by inhibiting TLR4/NF-?B pathway in rats
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články
PubMed
37159856
PubMed Central
PMC10226396
DOI
10.33549/physiolres.934978
PII: 934978
Knihovny.cz E-zdroje
- MeSH
- flavonoidy farmakologie terapeutické užití MeSH
- kolagen MeSH
- krysa rodu Rattus MeSH
- NF-kappa B MeSH
- oxid křemičitý toxicita MeSH
- plicní fibróza * chemicky indukované farmakoterapie prevence a kontrola MeSH
- silikóza * farmakoterapie MeSH
- toll-like receptor 4 MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- baicalin MeSH Prohlížeč
- flavonoidy MeSH
- kolagen MeSH
- NF-kappa B MeSH
- oxid křemičitý MeSH
- Tlr4 protein, rat MeSH Prohlížeč
- toll-like receptor 4 MeSH
Silicosis is an occupational lung disease caused by inhaling silica dust. The disease is characterized by early lung inflammation and late irreversible pulmonary fibrosis. Here we report the effect of Baicalin, a main flavonoid compound from the roots of Chinese herbal medicine Huang Qin on silicosis in a rat model. Results showed Baicalin (50 or 100 mg/kg/day) can mitigate the silica-induced lung inflammation and reduce the harm of alveolar structure and the blue region of collagen fibers in rat lung at 28 days after administration. At the same time, Baicalin also diminished the level of interleukin-1beta (IL-1beta, interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta1 (TGF-beta1) in lung tissues. The protein expression of collagen I (Col-1), alpha-smooth muscle actin (alpha-SMA) and vimentin were down-regulated while E-cadherin (E-cad) was increased in Baicalin-treated rats. In addition, the Toll Like Receptor 4 (TLR4)/ nuclear factor kappaB (NF-kappaB) pathway was enabled at 28 days after silica infusion, and the treatment of Baicalin diminished the expression of TLR4 and NF-?B in the lungs of rat with silicosis. These results suggested that Baicalin inhibited the pulmonary inflammatory and fibrosis in a rat model of silicosis, which could be attributed to inhibition of the TLR4/NF-kappaB pathway.
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