EFFECT OF DRUG TESTOSTERONE ON THE CONTENT OF RAGE AND INFLAMMATORY TRANSCRIPTION FACTOR NF-KB IN RAT TESTICULAR TISSUE WITH A FRUCTOSE-ENRICHED DIET

Abstract

Hypogonadism develops in diabetes mellitus (DM) and metabolic syndrome (MS). Testosterone replacement therapy can be applied, but its effect on spermatogenesis is controversial. Hyperglycemia promotes the accumulation of advanced glycation end products. Cellular receptors for advanced glycation end products (RAGE) trigger inflammatory responses through the proinflammatory transcription factor NF-kB. This signaling pathway may be involved in the disruption of spermatogenesis in hyperglycemia and during testosterone therapy.

The aim of the study is to evaluate the effect of testosterone on RAGE and NF-kB levels in rat’s testicles for DM and MS.

The data were obtained using Western blotting and immunofluorescence studies. The experiments were carried out on young rats. Animals were randomly divided into the groups: K (vivar control, 6), metabolic syndrome (MS, 5), metabolic syndrome + testosterone (MS + Tn, 8), testosterone (Tn, 4).

No significant changes in the content of RAGE and NF-kB in the testicular tissue of rats with hyperglycemia were found, which may be due to insufficient duration of hyperglycemia and mechanisms that inhibit inflammation.

The content of RAGE in testicular tissues was significantly higher in the MS + Tn and Tn groups (Western blotting) and in the MS + Tn group (immunofluorescence method). It is likely that testosterone, including against the background of hyperglycemia, causes an increase in the RAGE content in testicular tissue.

No significant changes in the NF-kB content in the testes were found. It seems that the inflammatory cascade realized with the participation of this factor is not activated in the testicles.

There are no significant changes in the testicular weight to body weight ratio and the lumen area to thickness area ratio of the seminiferous tubules. These facts indicate the absence of atrophic changes in the rat testes.

So, hyperglycemia for 6 weeks does not cause an increase in the RAGE and NF-kB levels in the rat testes; testosterone increases the RAGE content in the rat testicles both against the background of hyperglycemia and in the intact organism; despite the increase in RAGE, activation of the NF-kB-dependent proinflammatory cascade is not realized; atrophy in the testicular tissue of rats do not occur.