HMGB1 Box A gene therapy to alleviate bleomycin-induced pulmonary fibrosis in rats
Abstract Background Pulmonary fibrosis is characterized by the destruction of normal lung tissue and then replacement by abnormal fibrous tissue, leading to an overall decrease in gas exchange function. The effective treatment for pulmonary fibrosis remains unknown. The upstream pathogenesis of pulm...
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| Format: | Article |
| Language: | English |
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BMC
2025-01-01
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| Series: | BMC Pulmonary Medicine |
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| Online Access: | https://doi.org/10.1186/s12890-025-03522-2 |
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| author | Rathasapa Patarat Suchanart Chuaybudda Sakawdaurn Yasom Apiwat Mutirangura |
| author_facet | Rathasapa Patarat Suchanart Chuaybudda Sakawdaurn Yasom Apiwat Mutirangura |
| author_sort | Rathasapa Patarat |
| collection | DOAJ |
| description | Abstract Background Pulmonary fibrosis is characterized by the destruction of normal lung tissue and then replacement by abnormal fibrous tissue, leading to an overall decrease in gas exchange function. The effective treatment for pulmonary fibrosis remains unknown. The upstream pathogenesis of pulmonary fibrosis may involve cellular senescence of the lung tissue. Previously, a new gene therapy technology using Box A of the HMGB1 plasmid (Box A) was used to reverse cellular senescence and cure liver fibrosis in aged rats. Methods Here, we show that Box A is a promising medicine for the treatment of lung fibrosis. In a bleomycin-induced pulmonary fibrosis model in the male Wistar rats, Student’s t-test and one-way ANOVA were used to compare groups of samples. Results Box A effectively lowered fibrous tissue deposits (from 18.74 ± 0.62 to 3.45 ± 1.19%) and senescent cells (from 3.74 ± 0.40% to 0.89 ± 0.18%) to levels comparable to those of the negative control group. Moreover, after eight weeks, Box A also increased the production of the surfactant protein C (from 3.60 ± 1.68% to 6.82 ± 0.65%). Conclusions Our results demonstrate that Box A is a promising therapeutic approach for pulmonary fibrosis and other senescence-promoted fibrotic lesions. |
| format | Article |
| id | doaj-art-c1d16e257d104bc9adb6bd8e0449a523 |
| institution | Kabale University |
| issn | 1471-2466 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Pulmonary Medicine |
| spelling | doaj-art-c1d16e257d104bc9adb6bd8e0449a5232025-02-02T12:06:44ZengBMCBMC Pulmonary Medicine1471-24662025-01-0125111010.1186/s12890-025-03522-2HMGB1 Box A gene therapy to alleviate bleomycin-induced pulmonary fibrosis in ratsRathasapa Patarat0Suchanart Chuaybudda1Sakawdaurn Yasom2Apiwat Mutirangura3Center of Excellence in Molecular Genetics of Cancer and Human Diseases, Department of Anatomy, Faculty of Medicine, Chulalongkorn University, King Chulalongkorn Memorial HospitalCenter of Excellence in Molecular Genetics of Cancer and Human Diseases, Department of Anatomy, Faculty of Medicine, Chulalongkorn University, King Chulalongkorn Memorial HospitalDepartment of Microbiology, Faculty of Medicine, Chiang Mai UniversityCenter of Excellence in Molecular Genetics of Cancer and Human Diseases, Department of Anatomy, Faculty of Medicine, Chulalongkorn University, King Chulalongkorn Memorial HospitalAbstract Background Pulmonary fibrosis is characterized by the destruction of normal lung tissue and then replacement by abnormal fibrous tissue, leading to an overall decrease in gas exchange function. The effective treatment for pulmonary fibrosis remains unknown. The upstream pathogenesis of pulmonary fibrosis may involve cellular senescence of the lung tissue. Previously, a new gene therapy technology using Box A of the HMGB1 plasmid (Box A) was used to reverse cellular senescence and cure liver fibrosis in aged rats. Methods Here, we show that Box A is a promising medicine for the treatment of lung fibrosis. In a bleomycin-induced pulmonary fibrosis model in the male Wistar rats, Student’s t-test and one-way ANOVA were used to compare groups of samples. Results Box A effectively lowered fibrous tissue deposits (from 18.74 ± 0.62 to 3.45 ± 1.19%) and senescent cells (from 3.74 ± 0.40% to 0.89 ± 0.18%) to levels comparable to those of the negative control group. Moreover, after eight weeks, Box A also increased the production of the surfactant protein C (from 3.60 ± 1.68% to 6.82 ± 0.65%). Conclusions Our results demonstrate that Box A is a promising therapeutic approach for pulmonary fibrosis and other senescence-promoted fibrotic lesions.https://doi.org/10.1186/s12890-025-03522-2Idiopathic pulmonary fibrosisDNA damageDNA stabilityDNA protectionBox a of HMGB1Youth-DNA-gap |
| spellingShingle | Rathasapa Patarat Suchanart Chuaybudda Sakawdaurn Yasom Apiwat Mutirangura HMGB1 Box A gene therapy to alleviate bleomycin-induced pulmonary fibrosis in rats BMC Pulmonary Medicine Idiopathic pulmonary fibrosis DNA damage DNA stability DNA protection Box a of HMGB1 Youth-DNA-gap |
| title | HMGB1 Box A gene therapy to alleviate bleomycin-induced pulmonary fibrosis in rats |
| title_full | HMGB1 Box A gene therapy to alleviate bleomycin-induced pulmonary fibrosis in rats |
| title_fullStr | HMGB1 Box A gene therapy to alleviate bleomycin-induced pulmonary fibrosis in rats |
| title_full_unstemmed | HMGB1 Box A gene therapy to alleviate bleomycin-induced pulmonary fibrosis in rats |
| title_short | HMGB1 Box A gene therapy to alleviate bleomycin-induced pulmonary fibrosis in rats |
| title_sort | hmgb1 box a gene therapy to alleviate bleomycin induced pulmonary fibrosis in rats |
| topic | Idiopathic pulmonary fibrosis DNA damage DNA stability DNA protection Box a of HMGB1 Youth-DNA-gap |
| url | https://doi.org/10.1186/s12890-025-03522-2 |
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