AI Summary & Key Takeaways
AI InsightThe structure most resistant to diabetes-induced damage was the glomerulus, while the renal medullar and proximal renal tubule cells displayed damage and cicatrization.
📌 3 Key Takeaways
Abstract
To evaluate the effects of diabetes on nitric oxide synthase (NOS) activity and on gene expressions of B-cell lymphoma protein 2 (Bcl-2) and caspase-3 in the renal tissues of streptozotocin (STZ)-induced rats. Materials and methods: Twenty rats were analyzed in 2 equally distributed groups of healthy controls and STZ-induced diabetic rats. Rats with blood glucose levels of >=250 mg/dL were considered diabetic. Renal tissue sections were analyzed histomorphologically and immunohistochemically. Gene expressions of caspase-3 and Bcl-2 were evaluated by real-time quantitative polymerase chain reaction. Results: Bcl-2 expression significantly decreased in the diabetic group, both at the gene and protein level. Meanwhile, the expression of caspase-3 increased in the diabetic group, especially in proximal renal tubule cells. However, endothelial NOS (eNOS) protein expression in the glomerular endothelial nuclei was stronger in the control group, and protein expression of inducible NOS (iNOS) increased in the renal medullar area in the diabetic group. Conclusion: According to our results, hyperglycemia inhibits eNOS, leading to reduced nitric oxide production in endothelial cells. Inhibition of eNOS was correlated with glomerular cell loss due to apoptosis. Furthermore, increased expression of iNOS was associated with endothelial dysfunction in STZ-induced diabetic rats. The structure most resistant to diabetes-induced damage was the glomerulus, while the renal medullar and proximal renal tubule cells displayed damage and cicatrization.
Özet
To evaluate the effects of diabetes on nitric oxide synthase (NOS) activity and on gene expressions of B-cell lymphoma protein 2 (Bcl-2) and caspase-3 in the renal tissues of streptozotocin (STZ)-induced rats. Materials and methods: Twenty rats were analyzed in 2 equally distributed groups of healthy controls and STZ-induced diabetic rats. Rats with blood glucose levels of >=250 mg/dL were considered diabetic. Renal tissue sections were analyzed histomorphologically and immunohistochemically. Gene expressions of caspase-3 and Bcl-2 were evaluated by real-time quantitative polymerase chain reaction. Results: Bcl-2 expression significantly decreased in the diabetic group, both at the gene and protein level. Meanwhile, the expression of caspase-3 increased in the diabetic group, especially in proximal renal tubule cells. However, endothelial NOS (eNOS) protein expression in the glomerular endothelial nuclei was stronger in the control group, and protein expression of inducible NOS (iNOS) increased in the renal medullar area in the diabetic group. Conclusion: According to our results, hyperglycemia inhibits eNOS, leading to reduced nitric oxide production in endothelial cells. Inhibition of eNOS was correlated with glomerular cell loss due to apoptosis. Furthermore, increased expression of iNOS was associated with endothelial dysfunction in STZ-induced diabetic rats. The structure most resistant to diabetes-induced damage was the glomerulus, while the renal medullar and proximal renal tubule cells displayed damage and cicatrization.