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1.
Reprod Sci ; 31(7): 2092-2102, 2024 Jul.
Article in English | MEDLINE | ID: mdl-38532231

ABSTRACT

The present study investigates the changes in M1/M2 macrophage polarization resulting from unilateral testicular torsion in the bilateral testis. The study sample included 63 male Sprague-Dawley rats, which were randomly divided into nine groups (n = 7): Control, Sham (4 h (4 h), 24 h, 7 days (7d), 14d), and Torsion/Detorsion (T/D) (4 h, 24 h, 7d, 14d). Histopathological evaluations revealed no changes in the Sham groups, while T/D was noted to cause edema, vascular occlusion, disruption of seminiferous tubule epithelial organization, germ cell abnormalities and structural anomalies in the experimental rats, the severity and extent of which increased from 4 h to 14d after T/D. The Cosentino scores used to determine the degree of histological damage were consistent with the histopathological findings in all groups, while the Johnsen scores, as a marker of spermatogenesis, were lower in the T/D groups. Seminiferous tubule diameters and germinal epithelial thickness decreased significantly in parallel with increased tubule damage in the ipsilateral testicles. Testicular torsion significantly affected sperm motility, with significant reductions observed in the T/D 7d and T/D 14d groups. A hormone profile analysis revealed decreased testosterone levels in both the Sham and T/D groups when compared to the Controls. CD68 and CD163 immunoreactivities, as M1 and M2 macrophage surface markers, were determined in the testicular tissue using the avidin-biotin-peroxidase complex method. T/D interventions caused M1/M2 macrophage polarization changes and increased M1 macrophages, particularly in contralateral testicular tissue. The increase in M1 macrophages in contralateral testicular tissue following T/D in the present study suggests that cell processes, including macrophages, may play an important role in contralateral testicular injury.


Subject(s)
Macrophages , Rats, Sprague-Dawley , Spermatic Cord Torsion , Testis , Animals , Male , Spermatic Cord Torsion/pathology , Spermatic Cord Torsion/metabolism , Macrophages/metabolism , Macrophages/pathology , Testis/pathology , Testis/metabolism , Rats , Antigens, CD/metabolism , Sperm Motility , Antigens, Differentiation, Myelomonocytic/metabolism , Spermatogenesis/physiology , Cell Polarity , Receptors, Cell Surface/metabolism , CD68 Molecule
2.
Reprod Sci ; 30(10): 3103-3122, 2023 10.
Article in English | MEDLINE | ID: mdl-37171774

ABSTRACT

This study was carried out to investigate the protective properties of royal jelly on the testicular tissue of rats with testicular damage by giving fluoride. Sperm motility, epididymal sperm density and abnormal sperm ratios were examined and visualized with a light microscope. Expression levels of Caspase-3, Bcl-2, Nrf-2, NF-κB, COX-2, TNF-α and IL1-α proteins in testis tissue were determined by western blot technique. As a result of the study, MDA level, expression level of Bcl-2, NFÒ¡B, COX-2, TNF-α and IL1-α proteins, abnormal sperm rates were found higher in Fluoride-50 and Fluoride100 groups compared to other groups. In addition GSH, Catalase enzyme levels, expression levels of Caspase-3 and Nrf-2 proteins were found to be higher in Fluoride + Royal Jelly groups compared to Fluoride-50 and Fluoride-100 groups. In addition, lower degeneration of testicular tissue was found in the histological evaluation in the Fluoride + Royal Jelly groups compared to the other groups. When the data are evaluated royal jelly provides effective protection against testicular damage. From this point of view, we hope that similar results will be obtained when royal jelly is tested on humans.


Subject(s)
Infertility , Testis , Animals , Male , Rats , Antioxidants/pharmacology , Caspase 3/metabolism , Caspases/metabolism , Cyclooxygenase 2/metabolism , Fluorides/metabolism , Fluorides/pharmacology , Infertility/metabolism , Oxidative Stress , Proto-Oncogene Proteins c-bcl-2/metabolism , Semen/metabolism , Sperm Motility , Testis/metabolism , Transcription Factors/metabolism , Tumor Necrosis Factor-alpha/metabolism
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