Histological Investigation Of Experimentally Induced Diabetes Effects On The Distribution Of Transforming Growth Factor (Tgf Beta), Nuclear Factor Kappa B (Nf-Kappa B), Heat Schock 90 Beta (Hsp90 Beta) And E-Cadherin Proteins In Testicular Tissue

INTERNATIONAL JOURNAL OF MORPHOLOGY(2021)

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Abstract
Diabetes is a metabolic disorder characterized by high blood sugar levels and it causes complications in many systems, including the reproductive system. As a result of diabetic conditions, one of the mechanisms that can cause repression of reproductive activity is testicular oxidant stress. The identification of diabetes on the cell signaling molecules axis is still under discussion. The aim of this study was to detennine the effect of Transfonning Growth Factor (TGF beta), Nuclear Factor kappa B (NF-kappa B), Heat-schock 90 beta (HSP90 beta) signal pathways and E-cadherin cell adhesion molecule on infertility in diabetic rat testicular tissue. In our study, includes histological, molecular and biochemical analysis of testicular tissue removed at the end of the 2 weeks experiment period. A total of 14 adult male rats were divided as control and diabetes. No intervention was given to 7 male rats in the control group. For the diabetic group, 7 male rats were injected by intraperitoneal with a single dose of 55 mg/kg streptozotocin (STZ). TGF beta, NF-kappa B, HSP90 beta and E-cadherin proteins were immunohistochemically studied to investigate possible tissue damage, inflanunatoly process, cell stabilization and integrity due to diabetes. In order to determine oxidant stress, lipid peroxidation product malondialdehyde (MDA), glutathione (GSH) and glutathione peroxidase (GPx) analyzes were performed. Fibrosis, inflammatory changes and loss of spermatogenetic series are prominent findings in the diabetic group. On analysis of all the samples with immunostaining, in the diabetic group, TGF beta and NF-kappa B inununoexpression significantly increased, while Hsp90 beta and E-cadherin immunoexpression significantly decreased compared with control groups. Experimental diabetes was found to cause fibrosis, inflammation, disrupting cell adhesion and stabilization in testicular tissue. These results suggest that cellular therapy studies are needed for possible damage.
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Key words
Diabetes, Testis, TGF beta, Hsp90 beta, NF-kappa B, E-cadherin
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