Effects of hyperbaric oxygen therapy on clinical and economic outcomes in patients with deep second-degree burns.

Introduction: Deep second-degree burn injuries are the most challenging situations for the burn surgeon in the treatment of adult cases. While waiting for spontaneous closure increases the risk of hypertrophic scar and keloid, early excision and grafting pose the risk of donor site wound and permanent color differences. Unlike many studies in the literature, the current study was planned in a way to minimize factors other than burn wounds to investigate the effect of adding hyperbaric oxygen (HBO2) therapy to conventional treatment in deep second-degree burn wounds. Material and Methods: This prospective observational study included patients with burn injuries who underwent conventional treatment alone and those who underwent conventional plus HBO2 treatment performed by a single experienced surgeon and who met the study criteria. Results: Thirty-eight patients completed the study. Mean burned total body surface area (TBSA) was. 9.22 ± 3 43% (range 5% to 20%). There was no difference between the two groups in terms of age, burned TBSA, and burn etiology. The need for surgery and grafting was lower in patients who received HBO2 in addition to conventional treatment (p=0.003 and p=0.03, respectively). The patients in the HBO2 group had a shorter hospital stay, and their wounds epithelialized in a shorter time (p=0.169 and p≺0.001, respectively). They also had a higher satisfaction level and lower treatment cost (p=0.03 and p=0.36, respectively). Discussion: The results of this prospective study, in which co-factors were eliminated, showed that adding HBO2 to the conventional treatment of deep second-degree burns had a significant positive effect on patient outcomes, as well as reducing treatment costs.

Hypericum perforatum Attenuates Spinal Cord Injury-Induced Oxidative Stress and Apoptosis in the Dorsal Root Ganglion of Rats: Involvement of TRPM2 and TRPV1 Channels.

Oxidative stress and cytosolic Ca(2+) overload have important roles on apoptosis in dorsal root ganglion (DRG) neurons after spinal cord injury (SCI). Hypericum perforatum (HP) has an antioxidant property in the DRGs due to its ability to modulate NADPH oxidase and protein kinase C pathways. We aimed to investigate the protective property of HP on oxidative stress, apoptosis, and Ca(2+) entry through transient receptor potential melastatin 2 (TRPM2) and transient receptor potential vanilloid 1 (TRPV1) channels in SCI-induced DRG neurons of rats. Rats were divided into four groups as control, HP, SCI, and SCI + HP. The HP groups received 30 mg/kg HP for three concessive days after SCI induction. The SCI-induced TRPM2 and TRPV1 currents and cytosolic free Ca(2+) concentration were reduced by HP. The SCI-induced decrease in glutathione peroxidase and cell viability values were ameliorated by HP treatment, and the SCI-induced increase in apoptosis, caspase 3, caspase 9, cytosolic reactive oxygen species (ROS) production, and mitochondrial membrane depolarization values in DRG of SCI group were overcome by HP treatment. In conclusion, we observed a protective role of HP on SCI-induced oxidative stress, apoptosis, and Ca(2+) entry through TRPM2 and TRPV1 in the DRG neurons. Our findings may be relevant to the etiology and treatment of SCI by HP. Graphical Abstract Possible molecular pathways of involvement of Hypericum perforatum (HP) on apoptosis, oxidative stress, and calcium accumulation through TRPM2 and TRPV1 channels in DRG neurons of SCI-induced rats. The TRPM2 channel is activated by ADP-ribose and oxidative stress through activation of ADP-ribose pyrophosphate although it was inhibited by N-(p-amylcinnamoyl) anthranilic acid (ACA) and 2-aminoethyl diphenylborinate (2APB). The TRPV1 channel is activated by oxidative stress and capsaicin and it is blocked by capsazepine. Injury in the DRG can result in augmented ROS release, leading to Ca(2+) uptake through TRPM2 and TRPV1 channels. Mitochondria were reported to accumulate Ca(2+), provided intracellular Ca(2+) rises, thereby leading to depolarization of mitochondrial membranes and release of apoptosis-inducing factors such as caspase 3 and caspase 9. HP via regulation of NADPH oxidase and PKC inhibits TRPM2 and TRPV1 channels. The molecular pathway may be a cause of SCI-induced pain and neuronal death, and the subject should be urgently investigated.