MAPK immunoreactivity in streptozotocin-induced diabetic rat testis

Yelız Bozdemır Donmez1, Gulnur Kizilay2, Yeter Topcu-Tarladacalisir2

  • 1Department of Histology and Embryology, Faculty of Medicine, Namık Kemal University, Tekirdag, Turkey.

Acta Cirurgica Brasileira
|October 16, 2014
PubMed
Abstract

Insights

Experimental diabetes in male rats significantly alters testicular cell proliferation and key signaling pathways. Diabetic rats showed decreased extracellular signal-regulated kinase (ERK) and increased c-Jun NH2-terminal kinase (JNK) activity, suggesting a role in diabetes-induced infertility.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Reproductive Science

Background:

  • Diabetes mellitus is a complex metabolic disorder with known adverse effects on male reproductive function.
  • Mitogen-activated protein kinases (MAPKs) play crucial roles in cellular processes, including proliferation, differentiation, and apoptosis, within the testes.

Purpose of the Study:

  • To investigate the impact of experimental diabetes on the expression and activation of extracellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK) in male rat testes.
  • To assess the relationship between diabetes-induced alterations in these MAPK pathways and testicular cell proliferation.

Main Methods:

  • Male Sprague-Dawley rats were induced with experimental diabetes using streptozotocin (STZ).
  • Testicular tissue samples were collected after six weeks for light microscopy and immunohistochemical analysis.
  • Proliferating cell nuclear antigen (PCNA) index, total (t)-ERK, phosphor (p)-ERK, total (t)-JNK, and phosphor (p)-JNK immunoreactivities were quantified.

Main Results:

  • Diabetic rats exhibited a significant reduction in the PCNA index, indicating decreased cell proliferation.
  • Immunoreactivity for both total ERK (t-ERK) and phosphorylated ERK (p-ERK) was significantly decreased in diabetic testes.
  • While total JNK (t-JNK) levels remained unchanged, phosphorylated JNK (p-JNK) immunoreactivity was significantly elevated in diabetic rats.

Conclusions:

  • The observed decrease in t-ERK and p-ERK may be linked to reduced androgen levels in diabetic conditions.
  • Increased p-JNK suggests activation of the JNK pathway, potentially due to oxidative stress and inflammatory mediators associated with diabetes.
  • These MAPK pathway alterations may contribute to testicular apoptosis and subsequent infertility in diabetic males.

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