Abstract

Introduction: Idiopathic Pulmonary Fibrosis (IPF) is an intensifying respiratory disorder triggered by bleomycin in cancer patients, characterized by its lack of a definitive remedy. Bleomycin induces mitochondrial leakage and elevates Reactive Oxygen Species (ROS) in the pulmonary cavity, causing a reduction in glutathione (GSH), a vital lung antioxidant. This reduction in GSH levels, coupled with ROS's inactivation of the tumor suppressor gene p53, increases the chance of developing fibrosis. Although no antioxidant treatments that currently target these effects, Molecular Hydrogen Therapy (MHT) has proven effective in mitigating ROS in diseases like Chronic Obstructive Pulmonary Disease (COPD). This study aims to explore the impact of bleomycin-induced IPF on ROS and p53, investigating MHT as a potential treatment to alleviate oxidative stress in fibrosis. Methods: The experimental design includes four groups of mice, two receiving bleomycin injections and two receiving a control buffer solution. Within each subgroup, one group will undergo MHT, while the other will receive sterile air. Bronchoalveolar lavage will be used to measure GSH levels before and after MHT, and RNA sequencing will monitor p53 activity in all treatment and control groups. Results: Anticipated outcomes include elevated GSH levels in the MHT-treated bleomycin group, indicating an antioxidative effect. Consequently, improved p53 activity is expected compared to controls. Discussion: Anticipated results, based on existing literature, suggest that MHT enhances antioxidant defenses and modulates p53 activity, thereby reducing oxidative damage and fibrotic remodeling. These findings highlight the potential of MHT as a therapeutic intervention for IPF, with broader implications for managing other oxidative stress-mediated lung diseases. However, further research, including preclinical studies and clinical trials, is needed to validate these anticipated findings and ensure the long-term safety and efficacy of MHT in clinical practice. Conclusion: The study aims to replicate findings in human populations and proposes a paradigm shift in treating such diseases by addressing the root cause, ROS.

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