Ameliorative effect of selenium nanoparticles on testicular toxicity induced by cisplatin in adult male rats.

Cisplatin (Cis) is a treatment for testicular germ-cell tumors (TGCTs). Unfortunately, it causes testicular toxicity due to releasing reactive oxygen species (ROS) causing damage to testicular cells and chromosomes. The current study aimed to investigate the ameliorative effect of selenium nanoparticles (SeNPs) against cisplatin testicular toxicity in male rats by assessment of body weight, testis weight, oxidative stress markers in testis homogenates as (malondialdehyde (MDA), Superoxide dismutase (SOD), Glutathione reduced (GSH), Glutathione peroxidase (GSH âˆ¼ PX) and Catalase (CAT)), gene expression, testosterone concentration (T), sperm characteristics (count, motility and abnormality) and testicular histopathology. Methods: Thirty adult male rats divided equally into four groups; a single dose intraperitoneally injection of cisplatin (10 mg/kg) and selenium nanoparticles (2 mg/kg/day) were administrated alone or in combination. Cis group showed a decrease in body weight, testis weight, antioxidant activities (SOD, GSH, GSH âˆ¼ PX and CAT), T concentration and steroidogenetic expression, the data recorded an increase in MDA levels and sperm abnormality, meanwhile histopathology of testis sections showed degenerative changes in the seminiferous tubules. The co-administration of selenium nanoparticles ameliorated the harmful effects of cisplatin. In conclusion; SeNPs through its antioxidant potential may be useful to prevent the testicular toxicity induced by cisplatin to the rat testis by reducing oxidative stress.

Rapamycin-filgrastim combination therapy ameliorates portal hypertension-induced splenomegaly: Role of ß actin and S100A9 proteins modulation.

Objectives: Thioacetamide (TAA) was administered to induce an animal model of liver disease with secondary splenomegaly to assess the mechanisms underlying the effects of rapamycin and filgrastim when taken separately or in combination on the biochemical and histopathological aspects of the liver and spleen. Materials and Methods: Thirty adult male albino rats were divided into five groups (control, TAA-treated group, TAA+rapamycin, TAA+filgrastim, and TAA+rapamycin+filgrastim group). We measured relative liver and spleen weights, serum levels of alanine transaminase (ALT), aspartate transaminase (AST), and albumin. Molecular docking modeling and histopathological examination of liver and spleen sections with hematoxylin and eosin and Masson trichrome staining with immunohistochemical detection of splenic CD3 and CD20 lymphocytes, S100A9 and ß actin antibodies were detected. Morphometric and statistical analyses of the results were performed. Results: TAA administration altered the histological structure of the liver and spleen and impaired liver function. It increased the expression of splenic CD3, CD20 lymphocytes, and S100A9 while diminishing the expression of ß actin. Each of rapamycin and filgrastim, when administered separately, improved liver and spleen indices and liver function, but rapamycin did not affect the albumin level. They lowered splenic B and T lymphocyte levels. Expression levels of S100A9 showed down-regulation while ß actin levels were up-regulated when compared with TAA. Combination therapy improved liver and spleen tissue pathology and significantly ameliorated the expression of splenic lymphocytes through regulation of S100A9 and ß actin expression. Conclusion: The synergistic effect of combination therapy was dependent on the regulation of splenic S100A9 and ß actin levels.