Hyperbaric oxygen (HBO) therapy has emerged as a potential treatment, shown to enhance blood flow and angiogenesis. However, specific effects and mechanisms of HBO on limb ischaemia responding to a hypoxic environment remain largely unknown. We aimed to investigate the therapeutic potential of HBO in the treatment of limb ischaemia. Following limb ischaemia surgery, we evaluated the angiogenic capacity in wild-type C57BL/6J mice subjected to HBO treatment (100% oxygen at 3 ATA for 1 h/day for five consecutive days) compared to untreated controls. Notably, through laser Doppler perfusion imaging and CD31 staining mice receiving HBO postlimb ischaemia surgery exhibited significantly enhanced angiogenic capability and reduced ROS expression compared to nontreated counterparts. Additionally, in vitro experiments were conducted to investigate whether HBO could mitigate endothelial cell dysfunction and reactive oxygen species (ROS) production triggered by oxygen-glucose deprivation (OGD). HBO treatment rescued the impaired proliferation, migration and tube formation of endothelial cells following OGD. Mechanistically, HBO upregulated the expression of proangiogenic proteins, including vascular endothelial growth factor (VEGF), haem oxygenase-1 (HO-1), hypoxia-inducible factor 1 (HIF-1) and nuclear factor erythroid 2-related factor 2 (Nrf2). Collectively, HBO treatment shows promise in augmenting the endogenous angiogenic potential and suppressing ROS levels in limb ischaemia.
Keywords: HBO; ROS; angiogenesis; limb ischaemia.
© 2024 The Author(s). Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.