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Updated: Apr 17, 2026

Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis
Published on: May 9, 2025
Intervention of transforming pulmonary fibrosis with NF-κB p65 antisense oligonucleotide
Yan Zhou1, Ying-Ying Chen1, Xiao-Ye Zhang1
1Department of Respiratory, Shengjing Hospital of China Medical University Liaoning, China.
Objective:
NF-κB, especially p65 subunit, plays important role in the process of pulmonary fibrosis. In this study, we transformed fibroblast into myofibroblast induced by bleomycin, and then studied the effects of NF-κB p65 antisense oligonucleotide on pulmonary fibrosis in mouse model.
Methods:
Pulmonary fibrosis was induced by bleomycin in C57BL/6 mouse (modeling group). The NF-κB antisense oligonucleotide was injected intravenously into mouse 6 hours before inducing (test group), we performed broncho-alveolar lavage and blood collecting through cardiac puncture. Bronchoalveolar Lavage Fluid (BALF) and serum from normal C57BL/6 mouse (control group) were collected for comparison. Immunohistochemistry staining of the NF-κB and α-SMA on lung tissues and cultured cells were carried out in each group, respectively.
Results:
The expression level of NF-κB and α-SMA were both consistently higher in modeling group when compared with control group (P < 0.05). Meanwhile, they were reduced significantly through the intervention of NF-κB p65 antisense oligonucleotide in the test group (P < 0.05). More importantly, the expression of NF-κB was positively correlated with α-SMA.
Conclusion:
our study suggests the potential in prevention of bleomycin-induced pulmonary fibrosis with NF-κB p65 antisense oligonucleotide.
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