Diabetes leads to widespread complications including pancreatic β-cell damage, nephropathy and impaired wound healing. Hyperbaric oxygen therapy (HBOT) has been shown to improve wound healing through induction of ste...Diabetes leads to widespread complications including pancreatic β-cell damage, nephropathy and impaired wound healing. Hyperbaric oxygen therapy (HBOT) has been shown to improve wound healing through induction of stem cell recruitment and the potential to inhibit progression of diabetic complications. We aimed to determine the efficacy of HBOT in wound healing and organ preservation in a diabetic rat model. Diabetes was induced in male Wistar rats (n = 10/group) using streptozotocin (20 mg/kg sc) daily for 3 days. A wound was inflicted on the skin over the back and the rats were given HBOT (2.3 ATA for 1 h/day) for 1, 3, 5, 7 or 10 days or were not treated. Blood glucose, pancreatic β-cell damage, diabetic nephropathy and wound healing progression were assessed. Diabetic rats not treated with HBOT had significantly higher blood glucose levels compared to controls (26.7 ± 3.3 mmol/L vs. 5.8 ± 0.4 mmol/L;P ≤ 0.05). This was associated with significant increase in the percentage of β-cell damage (72% ± 9% vs. 10% ± 2%;P ≤ 0.05) and diabetic nephropathy. HBOT for 3 days and longer in diabetic rats reduced hyperglycemia to control levels. Pancreatic β-cell damage was negligible in rats treated with HBOT for 5 days and longer while diabetic nephropathy was diminished in animals treated for 10 days. Similarly HBOT induced wound healing and accelerated epithelial closure from 5 days of HBOT. In summary, our findings show the efficacy of HBOT in this diabetic rat model. There was significant reduction of hyperglycemia and inhibition of diabetic complications in the form of preservation of pancreatic and kidney structure and accelerated wound healing.展开更多
文摘Diabetes leads to widespread complications including pancreatic β-cell damage, nephropathy and impaired wound healing. Hyperbaric oxygen therapy (HBOT) has been shown to improve wound healing through induction of stem cell recruitment and the potential to inhibit progression of diabetic complications. We aimed to determine the efficacy of HBOT in wound healing and organ preservation in a diabetic rat model. Diabetes was induced in male Wistar rats (n = 10/group) using streptozotocin (20 mg/kg sc) daily for 3 days. A wound was inflicted on the skin over the back and the rats were given HBOT (2.3 ATA for 1 h/day) for 1, 3, 5, 7 or 10 days or were not treated. Blood glucose, pancreatic β-cell damage, diabetic nephropathy and wound healing progression were assessed. Diabetic rats not treated with HBOT had significantly higher blood glucose levels compared to controls (26.7 ± 3.3 mmol/L vs. 5.8 ± 0.4 mmol/L;P ≤ 0.05). This was associated with significant increase in the percentage of β-cell damage (72% ± 9% vs. 10% ± 2%;P ≤ 0.05) and diabetic nephropathy. HBOT for 3 days and longer in diabetic rats reduced hyperglycemia to control levels. Pancreatic β-cell damage was negligible in rats treated with HBOT for 5 days and longer while diabetic nephropathy was diminished in animals treated for 10 days. Similarly HBOT induced wound healing and accelerated epithelial closure from 5 days of HBOT. In summary, our findings show the efficacy of HBOT in this diabetic rat model. There was significant reduction of hyperglycemia and inhibition of diabetic complications in the form of preservation of pancreatic and kidney structure and accelerated wound healing.
