engleski

Influence of hyperbaric oxygenation on mRNA expression of antioxidative enzymes in blood vessels of male Sprague-Dawley rats

Introduction: Previously we showed (Mihaljevic et al. 2018) that acute hyperbaric oxygenation (A-HBO2) transiently impaired vasorelaxation due to increased oxidative stress but also that intermittent (4d-HBO2) hyperbaric treatments again increased vasorelaxation of rat aorta and furthermore brought the antioxidative status to the normal level in the macrocirculation. The present study assessed the effects of different types of HBO2 treatments on gene expression of antioxidative enzymes in cerebral microcirculation (brain blood vessels (BBVs)). Methods: 9-11-weeks old healthy male Sprague-Dawley rats were randomly assigned to the following groups (n=6-8 rats/group): CONTROL group (intact animals), and 2 hyperbaric groups that received either single (A-HBO2) or intermitent (4 consecutive HBO2 treatments, one per day, 4d-HBO2) hyperbaric treatments. The therapy protocol consists of 120- minute sessions of 100% O2 at 2.0 bars absolute of pressure. Following the protocol, rats were anesthetized with ketamine (75 mg/kg) and midazolam (2.5 mg/kg) and sacrificed by decapitation. All surface BBVs were isolated and collected for mRNA levels measurements of antioxidative ezymes. Data were analyzed using One-Way ANOVA, present as mean±SD and p<0.05 was considered significant. Results: The A-HBO2 (0.49±0.19) group had significantly decreased level of MnSOD compared to CONTROL group (0.95±0.19). Expression of EC-SOD in 4d-HBO2 group (1.75±0.43) was significantly increased compared to CONTROL (0.60±0.20) and A-HBO2 (0.85±0.53) groups. GPx1 was significantly decreased in A-HBO2 group (0.54±0.22) compared with the CONTROL (1.23±0.38) and 4d-HBO2 (1.07±0.43) groups. GPx4 was significantly increased in A-HBO2 and 4d-HBO2 compared to CONTROL group (p<0.05). CAT was significantly decreased in both HBO2 groups (p<0.05) compared to CONTROL group. Discussion: A-HBO2 significant reduced antioxidant enzymes in BBVs, mostly compared to the untreated group, which results in reduced antioxidant status in the A-HBO2 group. Re-improving antioxidative status with prolonged exposure to hyperbaric therapy is the consequence of increased EC-SOD and GPx1 gene expression in BBV. Conclusion: A-HBO2 leads to a significantly antioxidative status reduction in the microcirculation resulting in increased oxidative stress. On the other hand, 4d-HBO2 has beneficiary effects on the antioxidative capacity of cerebral microvessels.

hyperbaric oxygenation ; oxidative stress ; antioxidative ezymes ; Sprague-Dawley rats

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