Schistosomiasis is a parasitic disease and it associated with erectile dysfunction and infertility while possesses anti-oxidant properties. This study evaluates to protect the male fertility, and to preserve sperm quality in ()-infected mice. A 36 male albino mice of six equal sets were used in the study each with 6 mice; Control, cupressuflavone (200 mg/kg), and () (80 mg/kg), infected mice, cupressuflavone (200 mg/kg) infected mice, and (80 mg/kg) infected mice for 4 weeks. Serum testosterone, luteinizing hormone, follicle stimulating hormone, dehydroepiandrosterone sulfate, and Sex hormone binding globulin were determined. Glucose-6-phosphate dehydrogenase, 3β-hydroxysteroid dehydrogenase, total protein, and cholesterol in testis were detected. Antioxidants and sodium/potassium-ATPase in the hypothalamus, testis, and sperm were identified. Sperm counts, motility, and abnormality, as well as, sperm monoclonal proliferating antibody Ki-67 were evaluated. The results revealed that decreased superoxide dismutase, glutathione, serum testosterone and dehydroepiandrosterone sulfate, sperm count and motility, sodium/potassium-ATPase activity while increased malondialdehyde, serum follicle stimulating hormone, sex hormone binding globulin, and luteinizing hormone, glucose-6-phosphatedehydrogenase, 3β-hydroxysteroid dehydrogenase, cholesterol, total protein, sperm abnormality, the percentage of spermatogonia, 1st spermatocyte, 2nd spermatocyte, and spermatid in the testis. Also, and cupressuflavone oral administration to -infected group back all of the aforementioned parameters to be close control values where had an efficient impact than cupressuflavone did. In conclusion, sustains testosterone cycle and sperm quality in -related testicular dysfunction.
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http://dx.doi.org/10.1007/s12639-024-01730-x | DOI Listing |
Mesenchymal stem/stromal cells (MSCs) offer promising therapeutic potential in cell-based therapies for various diseases. However, the safety of genetically modified MSCs remains poorly understood. This study aimed to evaluate the general toxicity and safety of Wharton's Jelly-Derived MSCs (WJ-MSCs) engineered to express the antimicrobial peptide SE-33 in an animal model.
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Michael Smith Laboratories, University of British Columbia, Vancouver, British Columbia, Canada.
an invasive basidiomycete fungal pathogen, causes one of the most prevalent, life-threatening diseases in immunocompromised individuals and accounts for ~19% of AIDS-associated deaths. Therefore, understanding the pathogenesis of and its interactions with the host immune system is critical for developing therapeutics against cryptococcosis. Previous studies demonstrated that cells lacking polyphosphate (polyP), an immunomodulatory polyanionic storage molecule, display altered cell surface architecture but unimpaired virulence in a murine model of cryptococcosis.
View Article and Find Full Text PDFPertussis resurged over the last decade in most countries that replaced the traditional whole-cell pertussis vaccines (wP) by the less reactogenic acellular pertussis vaccines (aP). The aP vaccines induce a Th2-polarized immune response and by a yet unknown mechanism hamper the clearance of from infected nasopharyngeal mucosa. The aP-induced pertussis toxin-neutralizing antibodies effectively prevent the life-threatening pertussis pneumonia in infants, but aP-elicited immunity fails to prevent infection of nasopharyngeal mucosa and transmission of .
View Article and Find Full Text PDFmBio
March 2025
College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, China.
Membrane-associated RING-CH-type finger (MARCH) proteins, a class of E3 ubiquitin ligases, have been reported to be involved in the infection of multiple viruses and the regulation of type I interferon (IFN) production. However, the specific role and mechanisms by which MARCH proteins influence Japanese encephalitis virus (JEV) infection remain poorly understood. Here, we systematically investigate the functional relevance of MARCH proteins in JEV replication by examining the effects of siRNA-mediated knockdown of MARCHs on viral infection.
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