糖尿病と臨床実践のジャーナル

抽象的な

The Development of Cellular Oxidative Injury due to Ongoing Diabetes Requirements Implant of the Pancreas

Tarunkanti Mondal

There is a lot of evidence that hyperglycaemia-induced cellular oxidative stress is a major factor in the onset and progression of chronic diabetic lesions. In this study, we determined whether pancreas transplantation prevented the imbalance between the lungs of diabetic rats' antioxidant defences and the excessive production of reactive oxygen species. After four and twelve weeks of follow-up, each group was further divided into two subgroups of ten rats each. These subgroups were then killed. All rats had their plasma glucose, glycosylated hemoglobin, and insulin levels measured. In the pulmonary tissue of all of the rats, the concentrations of lipid hydro peroxide as well as the activities of superoxide dismutase, catalase, and glutathione peroxidase enzymes were measured. The DC rodents showed raised blood glucose and glycosylated hemoglobin levels, with insulin blood levels altogether lower than the NC rodents. They likewise showed altogether expanded LPO focuses in the lungs following 4 and 12 weeks of followup. SOD, CAT, and GSH-Px antioxidant activities, on the other hand, decreased significantly during these times 12 weeks after diabetes induction. Effective PT adjusted all clinical and metabolic changes in the diabetic rodents, with supported normoglycemia all through the review. Four weeks after PT, low SOD, CAT, and GSH-Px antioxidant activities and excessive lung LPO production were back to normal. In diabetic rats, PT can reduce oxidative stress in the pulmonary tissue. It may serve as the foundation for preventing lungs with chronic diabetic lesions.