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.
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.
Authors: Brigham C Willis; Janice M Liebler; Katherine Luby-Phelps; Andrew G Nicholson; Edward D Crandall; Roland M du Bois; Zea Borok Journal: Am J Pathol Date: 2005-05 Impact factor: 4.307
Authors: Jeong-Hyung Lee; Jin Kyu Choi; Min Soo Noh; Bang Yeon Hwang; Young Soo Hong; June Joon Lee Journal: Planta Med Date: 2004-06 Impact factor: 3.352
Authors: Phuong-Thu T Pham; Phuong-Chi T Pham; Gabriel M Danovitch; David J Ross; H Albin Gritsch; Elizabeth A Kendrick; Jennifer Singer; Tariq Shah; Alan H Wilkinson Journal: Transplantation Date: 2004-04-27 Impact factor: 4.939