Mehmet Akif BAKTIR, Sinem ÖNEM, Burcu BARAN, Ali Sefa MENDİL, Mustafa ÖZKARACA, Ahmet CUMAOĞLU
Clinical and Experimental Health Sciences - 2025;15(4):906-911
Objective: This study examined the efficacy of hyperbaric oxygen therapy (HBOT) in facilitating recovery from high fructose-induced pulmonary fibrosis in rats and explored the underlying mechanisms. Methods: Male Wistar rats were randomly divided into four groups: Control (standard diet for 10 weeks), High fructose diet (HFD, for 10 weeks), Hyperbaric oxygen therapy (HBOT standard diet with 2.4 ATA (atmospheric pressure absolute) for 1 hr. during weeks 9-10) and HFD+HBOT (High fructose diet with 2.4 ATA for one h during weeks 9-10). Histopathological alterations, including mononuclear cell infiltration and hyperemia were determined by Hematoxylin and Eosin staining. Fibrosis was evaluated using Masson's trichrome staining. Markers of autophagy (LC3B: Microtubule-associated protein light chain 3B, Beclin-1) and inflammation (COX-1: Cyclooxygenase-1) were examined using immunohistochemical staining. Results: In rats, a high-fructose diet caused interstitial fibrosis, hyperemia, and mononuclear cell infiltration in the lung tissues. Additionally, HFD boosted the production of the proinflammatory COX-1 protein and autophagic LC3B and Beclin-1. The outcomes were comparable to those of the control group in rats administered hyperbaric oxygen therapy alone. Mononuclear cell infiltration, hyperemia, and fibrosis, along with autophagic and inflammatory markers, were markedly attenuated in the HFD+HBOT group. Conclusion: The key finding of our study is that HBOT effectively mitigates the development of pulmonary fibrosis in rats fed a HFD. These findings underscore the potential of HBOT as a promising therapeutic intervention for managing pulmonary fibrosis associated with metabolic disorders.
