Background
Pressure ulcer (PU) is a tissue necrosis disorder in which the cutaneous structures are affected by pressure and shear stress, leading to ischemia and circulatory impairment, etc. Increased oxidative stress caused by ischemia and reperfusion has been reported to contribute to the pathogenesis of the disease. Aldehyde reductase (ALR) is an NADPH-dependent detoxification enzyme encoded by AKR1A and involved in the synthesis of ascorbic acid (AsA). ALR deficiency results in inadequate detoxification of carbonyl compounds, which may cause organ damage AsA is extremely reactive to radical species and functions as an antioxidant. In this study, we analyzed the effect of AKR1A on pressure ulcer formation.
Methods
Ischemia-reperfusion injury (IRI) in the skin of AKR1A knockout (KO) and wild-type control (WT) mice was compared grossly and histologically. Next, the effects of AsA administration on tissue injury of IRI in KO and WT were examined. We also examined the effects of AsA administration on viable cells in hypoxia/reoxygenation load (H/R) using mouse fibroblasts.
Result and Discussion
AKR1A deficiency aggravates pressure ulcer formation, and AsA may attenuate tissue injury caused by IRI and H/R. Since AsA is a free radical scavenger, it is possible that reactive oxygen species are involved in the aggravation of pressure ulcer formation and that AsA may be beneficial in the reduction of pressure ulcer severity. We are currently investigating expression changes of tissue injury-related molecules associated with ischemia-reperfusion, and will report on these findings as well.