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Icotinib Improves Bleomycin-Induced Pulmonary Fibrosis by Inhibiting Epithelial-Mesenchymal Transition of Alveolar Epithelial Cells
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Wenqi XU1, Lei XIAO1, Wei XU2, Jingjing YAN3, Wenqiang GU3, Xianwei LI3, *
Chinese Pharmaceutical Journal | 2024, 59(12) : 1120 - 1128
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Chinese Pharmaceutical Journal | 2024, 59(12): 1120-1128
Icotinib Improves Bleomycin-Induced Pulmonary Fibrosis by Inhibiting Epithelial-Mesenchymal Transition of Alveolar Epithelial Cells
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Wenqi XU1, Lei XIAO1, Wei XU2, Jingjing YAN3, Wenqiang GU3, Xianwei LI3, *
Affiliations
  • 1 Dongcheng District, the First Affiliated Hospital of Anhui Medical University, Hefei 230000, China
  • 2 Department of Urology, The Second Affiliated Hospital of Wannan Medical College, Wuhu 241000, China
  • 3 Department of pharmacology, Wannan Medical College, Wuhu 241002, China
Published: 2024-06-22 doi: 10.11669/cpj.2024.12.007
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OBJECTIVE This study aimed to investigate the role and potential mechanisms of Icotinib (ICO) on pulmonary fibrosis. METHODS C57BL/6 mice were randomly divided into Sham group, PF group, ICO 30 mg·kg-1 group and ICO 60 mg·kg-1 group, 8 rats in each group. A mouse model of PF was induced by intratracheal injection of bleomycin (3 mg·kg-1). Hematoxylin-eosin staining and Masson trichrome staining for lung tissues were performed to observe the pathological alterations and collagen deposition. Immunohistochemical detection of lung tissue collagen type Ⅰ (collagen Ⅰ) expression. In vitro, the lung epithelial cells were divided into control group, epidermal growth factor (EGF) group, EGF combined with ICO (0.1, 1, 10 mmol·L-1) groups. The protein expression of E-cadherin, α-SMA and nuclear transfer of NF-κB p65 were detected by immunofluorescence. The protein levels of Collagen Ⅰ, E-cadherin, α-SMA, Vimentin, phosphorylation epidermal growth factor receptor (p-EGFR), p-IκBα, p-NF-κB p65 and nuclear NF-κB p65 were detected by Western blot analysis in lung tissue and (or) cells. RESULTS The results demonstrated that ICO inhibited bleomycin-induced collagen deposition, reduced type Ⅰ collagen expression, alleviated bleomycin-induced EMT (increased E-cadherin expression and decreased Vimentin and α-SMA expression), and decreased phosphorylation of EGFR, IκBα, NF-κB p65 and nuclear translocation of NF-κB p65 in vivo. Furthermore, incubation of lung epithelial cells with EGF activated EMT and EGFR/NF-κB signaling pathway, and these effects were reversed by ICO In vitro. CONCLUSION In conclusion, ICO attenuates EGF-induced EMT in lung epithelial cells and bleomycin-induced pulmonary fibrosis in mice by downregulating EGFR/NF-κB pathway.

Icotinib  /  Pulmonary fibrosis  /  epithelial-mesenchymal transition  /  EGFR/NF-κB signaling pathway
Wenqi XU, Lei XIAO, Wei XU, Jingjing YAN, Wenqiang GU, Xianwei LI. Icotinib Improves Bleomycin-Induced Pulmonary Fibrosis by Inhibiting Epithelial-Mesenchymal Transition of Alveolar Epithelial Cells[J]. Chinese Pharmaceutical Journal, 2024 , 59 (12) : 1120 -1128 . DOI: 10.11669/cpj.2024.12.007
Year 2024 volume 59 Issue 12
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doi: 10.11669/cpj.2024.12.007
  • Receive Date:2023-12-22
  • Online Date:2025-11-25
  • Published:2024-06-22
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  • Received:2023-12-22
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Affiliations
    1 Dongcheng District, the First Affiliated Hospital of Anhui Medical University, Hefei 230000, China
    2 Department of Urology, The Second Affiliated Hospital of Wannan Medical College, Wuhu 241000, China
    3 Department of pharmacology, Wannan Medical College, Wuhu 241002, China
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表12种不同金属材料的力学参数

Family
属数
Number of
genus
种数
Number of
species
占总种数比例
Percentage of
total species (%)

Genus
种数
Number of
species
占总种数比例
Percentage of total
species (%)
鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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