Abstract

Testosterone, the production of which is stimulated by the release of luteinizing hormone (LH) has a remarkable anti-inflammatory and immunomodulatory effect, and in conditions of testosterone deficiency tissue damage can occur due to excessive differentiation of macrophages into a pro-inflammatory M1 phenotype. The aim of this study was to determine the spread of CD68 receptorn as the marker of inflammation on the cells in the interstitial space and testicular vessels under LH synthesis blockade with tryptorelin. Sexually mature white male rats were randomly divided into control (10 animals) and experimental (25 animals) groups. Animals in the experimental group were injected with a tryptorelin acetate solution (0.3 mg/kg). Immunochemical analysis of CD68+ expression was estimated at Olympus FV10i-LIV laser scanning confocal microscope using fluorescent labeling dye hilyte flour 488. It was shown that luteinizing hormone deprivation led to an increase in the distribution of the CD68 receptor in the interstitial space and in the testicular vessels from day 30 to 180 of the experiment, associated with the increase of inducible NO synthase activity in testis tissue. Keywords: CD68, luteinizing hormone, macrophage M1 phenotype, testis, testosterone, tryptorelin

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