HBOT2 Preconditioning Prevents Endothelial Dysfunction through Increased Sirt-1
نویسندگان
1 Department of Clinical Pathology, Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia.
2 Doctoral Program of Medical Science, Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia
3 Department of Medical Physiology and Biochemistry, Faculty of Medicine, Universitas Airlangga, Surabaya, Indonesia
doi
10.26655/JMCHEMSCI.2024.12.21چکیده
The role of Sirt-1, a molecule that regulates transcription factors such as NF-kB and eNOS and is potentially linked to endothelial dysfunction during diving, has not been previously investigated. The study aims to determine the impact of HBO2 preconditioning on Sirt-1 and eNOS in preventing endothelial dysfunction in diving. This study is a true experimental post-test design using forty male Sprague Dawley rats. Diving was carried out in an animal chamber. All data were collected 12 and 24 hours after decompression diving. Endothelial Sirt-1 expression differed significantly between control and treatment groups only at 12 hours after diving (p = 0.049), and both groups exhibited notable increases after 24 hours (p < 0.001, p < 0.001). After 12 and 24 hours, the expression of eNOS in endothelial cells was similar across the treatment and control groups (p = 0.406 and 0.326, respectively). However, only the treatment group displayed a substantial increase in eNOS expression (p = 0.041). Twenty-four hours after diving, VCAM-1 levels differed between the treatment and control groups (p = 0.014), and the control group experienced a substantial decrease (p = 0.014). The control and treatment groups displayed comparable levels of endothelial NF-kB expression at any time, but the changes were significant in the control group (p = 0.007). This study suggests that HBO2 preconditioning increases Sirt-1 and eNOS and decreases NF-kB. However, the decrease in NF-kB levels was not followed by a decrease in VCAM-1. This indicates that HBO2 preconditioning prolongs the duration of endothelial dysfunction despite a decrease in its transcription factors expression and an increase in antioxidant enzyme levels. Further research is required to explore other mechanisms involved in preventing endothelial dysfunction through HBO2 preconditioning.