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    Does Chrysin prevent severe lung damage in Hyperoxia-Induced lung injury Model?
    (Elsevier, 2021) Ozdemir, Ramazan; Gokce, Ismail Kursat; Taslidere, Asli Cetin; Tanbek, Kevser; Gul, Cemile Ceren; Sandal, Suleyman; Turgut, Hatice
    Background: Oxidative stress and inflammation play a critical role in the etiopathogenesis of bronchopulmonary dysplasia (BPD). The aim of this study was to evaluate the preventive effect of Chrysin (CH), an antioxidant, antiinflammatory, antiapoptotic and antifibrotic drug, on hyperoxia-induced lung injury in a neonatal rat model. Methods: Forty infant rats were divided into four groups labeled the Control, CH, BPD, and BPD + CH. The control and CH groups were kept in a normal room environment, while the BPD and BPD + CH groups were kept in a hyperoxic (90-95%) environment. At the end of the study, lung tissue was evaluated with respect to apoptosis, histopathological damage and alveolar macrophage score as well as oxidant capacity, antioxidant capacity, and inflammation. Results: Compared to the BPD + CH and control groups, the lung tissues of the BPD group displayed substantially higher levels of MDA, TOS, TNF-alpha, and IL-1 beta (p < 0.05). While the BPD + CH group showed similar levels of TNF-alpha, and IL-1 beta as the control group, MDA and TOS levels were higher than the control group, and significantly lower than the BPD group (p < 0.05). The BPD group exhibited considerably lower levels of TAS, SOD, GSH, and GSHPx in comparison to the control group (p < 0.05). The BPD and BPD + CH groups exhibited higher mean scores of histopathological damage and alveolar macrophage when compared to the control and CH groups (p <= 0.0001). Both scores were found to be lower in the BPD + CH group in comparison to the BPD group (p <= 0.0001). The BPD + CH group demonstrated a significantly lower average of TUNEL and caspase-3 positive cells than the BPD group. Conclusion: We found that prophylaxis with CH results in lower histopathological damage score and reduces apoptotic cell count, inflammation and oxidative stress while increasing anti-oxidant capacity.
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    Molsidomine decreases hyperoxia-induced lung injury in neonatal rats
    (Springernature, 2023) Aslan, Mehmet; Gokce, Ismail Kursat; Turgut, Hatice; Tekin, Suat; Taslidere, Asli Cetin; Deveci, Mehmet Fatih; Kaya, Huseyin
    BackgroundThe study's objective is to evaluate if Molsidomine (MOL), an anti-oxidant, anti-inflammatory, and anti-apoptotic drug, is effective in treating hyperoxic lung injury (HLI).MethodsThe study consisted of four groups of neonatal rats characterized as the Control, Control+MOL, HLI, HLI + MOL groups. Near the end of the study, the lung tissue of the rats were evaluated with respect to apoptosis, histopathological damage, anti-oxidant and oxidant capacity as well as degree of inflammation.ResultsCompared to the HLI group, malondialdehyde and total oxidant status levels in lung tissue were notably reduced in the HLI + MOL group. Furthermore, mean superoxide dismutase, glutathione peroxidase, and glutathione activities/levels in lung tissue were significantly higher in the HLI + MOL group as compared to the HLI group. Tumor necrosis factor-alpha and interleukin-1 beta elevations associated with hyperoxia were significantly reduced following MOL treatment. Median histopathological damage and mean alveolar macrophage numbers were found to be higher in the HLI and HLI + MOL groups when compared to the Control and Control+MOL groups. Both values were increased in the HLI group when compared to the HLI + MOL group.ConclusionsOur research is the first to demonstrate that bronchopulmonary dysplasia may be prevented through the protective characteristics of MOL, an anti-inflammatory, anti-oxidant, and anti-apoptotic drug.ImpactMolsidomine prophylaxis significantly decreased the level of oxidative stress markers.Molsidomine administration restored the activities of antioxidant enzymes.Molsidomine prophylaxis significantly reduced the levels of inflammatory cytokines.Molsidomine may provide a new and promising therapy for BPD in the future.Molsidomine prophylaxis decreased lung damage and macrophage infiltration in the tissue.
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    The protective effects of apocynin in hyperoxic lung injury in neonatal rats
    (Wiley, 2022) Ozdemir, Ramazan; Gokce, Ismail Kursat; Tekin, Suat; Taslidere, Asli Cetin; Turgut, Hatice; Tanbek, Kevser; Gul, Cemile Ceren
    Aim Inflammation and oxidate stress are significant factors in the pathogenesis of bronchopulmonary dysplasia (BPD). The aim of this study is to investigate the efficacy of apocynin (APO), an anti-inflammatory, antioxidant, and antiapoptotic drug, in the prophylaxis of neonatal hyperoxic lung injury. Method This experimental study included 40 neonatal rats divided into the control, APO, BPD, and BPD + APO groups. The control and APO groups were kept in a normal room environment, while the BPD and BPD + APO groups were kept in a hyperoxic environment. The rats in the APO and BPD + APO groups were administered intraperitoneal APO, while the control and BPD rats were administered ordinary saline. At the end of the trial, lung tissue was evaluated with respect to the degree of histopathological injury, apoptosis, oxidant and antioxidant capacity, and severity of inflammation. Result The BPD and BPD + APO groups exhibited higher mean histopathological injury and alveolar macrophage scores compared to the control and APO groups. Both scores were lower in the BPD + APO group in comparison to the BPD group. The BPD + APO group had a significantly lower average of TUNEL positive cells than the BPD group. The lung tissue examination indicated significantly higher levels of mean malondialdehyde (MDA), total oxidant status (TOS), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 beta (IL-1 beta) in the BPD group compared to the control and APO groups. While the TNF-alpha and IL-1 beta levels of the BPD + APO group were similar to that of the control group, the MDA and TOS levels were higher compared to the controls and lower compared to the BPD group. The BPD group demonstrated significantly lower levels/activities of mean total antioxidant status, glutathione reductase, superoxide dismutase, glutathione peroxidase in comparison to the control and APO groups. While the mean antioxidant enzyme activity of the BPD + APO group was lower than the control group, it was significantly higher compared to the BPD group. Conclusion This is the first study in the literature to reveal through an experimental neonatal hyperoxic lung injury that APO, an anti-inflammatory, antioxidant, and antiapoptotic drug, exhibits protective properties against the development of BPD.