This work aimed to investigate the role of diabetes on cell proliferation, and apoptosis in testis. The rats were randomly allotted into one of two experimental groups: control and diabetic group; each group contain 10 animals. Diabetes was induced by a single intraperitoneal injection of STZ (50 mg/kg). Testicular damage was examined by using hematoxylin and eosin, immunohistochemical staining of proliferating cell nuclear antigen (PCNA), and apoptosis was determined by terminal-deoxynucleotidyl-transferase mediated dUTP nick end labeling (TUNEL). Potential disorders associated with seminiferous tubular sperm formation were evaluated using the Johnsen score. The mean seminiferous tubule diameter (MSTD) and mean testicular biopsy score (MTBS) values were significantly decreased in diabetic group was compared to the control group. Our data indicate a significant reduction in the expression of PCNA and an enhancement in the activity of TUNEL in testis tissues of the diabetic group. The effects of diabetes on spermatogenesis can be clearly detected as a testicular cell death and decrease in MTBS, MSTD, and PCNA expression.
ARTICLE INFO ABSTRACTThe aim of this study was to investigate the caspase-3 activity in neuronal apoptosis after experimental closed head trauma model in rats. Twenty adult male rats were randomly divided into two groups: control and trauma groups. In trauma group, a cranial impact was delivered to the skull from a height of 7 cm at a point just in front of the coronal suture and over the right hemisphere. Rats were sacrificed at 12 hours after the onset of injury. Brain tissues were removed for histopathological investigation. In the trauma group, the neurons became extensively dark and degenerated into picnotic nuclei. The number of apoptotic neurons in frontal cortex tissue of trauma group was significantly more than control groups. In conclusion, the caspase 3 immunopositivity was increased in degenerating neurons of the frontal cortex tissue following trauma. The present results indicate that closed head trauma caused degenerative changes and increased caspase 3 immonupositivity in neurons.
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