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1.
Biomed Pharmacother ; 79: 44-51, 2016 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-27044811

RESUMEN

Propolis is an adhesive substance which is collected and used by honeybees. Propolis is a potent antioxidant and a free radical scavenger. This study was designed to determine whether propolis could protect against dysfunction and oxidative stress induced by methotrexate-induced injury in rat testis. A total of 40 male Wistar albino rats were divided into four groups: group 1 was the untreated control. On the eighth day of the experiment, groups 2 and 3 received single intraperitoneal injections of methotrexate (MTX) at 20mg/kg. Groups 3 and 4 received 100mg/kg/day propolis (by oral gavage) for 15 days by the first day of the experimental protocol. Then the rats were decapitated under anesthesia, and their testes were removed. The histopathological and biochemical analysis along with apoptosis assessment of testis tissues were compared. Immunohistochemical analysis of Heat shock protein-70 (HSP-70) and Proliferating Cell Nuclear Antigen (PCNA) were performed. The phenolic characterization of propolis was performed by Liquid chromatography-mass spectrometry (LC-MS/MS). Methotrexate caused tended to increase in malondialdehyde level and in the number of apoptotic cells; it also caused a decrease in MSTD and JTBS, PCNA and HSP-70 expression and xanthine oxidase levels in group 2. Propolis prevented the rise in malondialdehyde, xanthine oxidase levels and HSP-70 expression and improved testicular morphology and JTBS. It was found that, methorexate gives rise to serious damage in the testes and propolis is a potent antioxidant agent in preventing testicular injury.


Asunto(s)
Metotrexato/efectos adversos , Própolis/farmacología , Sustancias Protectoras/farmacología , Testículo/patología , Animales , Apoptosis/efectos de los fármacos , Proteínas HSP70 de Choque Térmico/metabolismo , Inmunohistoquímica , Etiquetado Corte-Fin in Situ , Masculino , Malondialdehído/metabolismo , Fenoles , Antígeno Nuclear de Célula en Proliferación/metabolismo , Ratas Wistar , Túbulos Seminíferos/efectos de los fármacos , Túbulos Seminíferos/patología , Testículo/efectos de los fármacos , Testículo/metabolismo , Xantina Oxidasa/metabolismo
2.
Syst Biol Reprod Med ; 62(1): 22-30, 2016.
Artículo en Inglés | MEDLINE | ID: mdl-26566682

RESUMEN

Diabetes is known to be associated with erectile dysfunction, retrograde ejaculation, level of testicular hormone, and a decrease in semen quality, respectively. In this project, we aimed to investigate at the molecular level, the effects of NOS on testes pathology in diabetes and examine the effects of pentoxifylline on healing. A total of 50 Wistar albino male rats were divided into five groups: Group I control; Group II only diabetes; Group III and IV diabetes + pentoxifylline; Group V only pentoxifylline. Group III rats received 50 mg/kg/day pentoxifylline during two months. In comparison, Group IV rats received saline in the first month followed by 50 mg/kg/day of pentoxifylline for the following month. NOS expression in testicular tissue was assessed using qRT-PCR, western blot, and immunohistochemistry. The mean seminiferous tubule diameter, Johnsen's testicular biopsy score, and serum testosterone levels decreased compared to controls. In contrast, the number of apoptotic cells, the levels of nNOS, iNOS and eNOS mRNA, and protein increased when compared to the control. Upon pentoxifylline therapy NOS decreased suggesting that it contributes to this damage and treatment with pentoxifylline may be effective in reversing this damage.


Asunto(s)
Diabetes Mellitus Experimental/tratamiento farmacológico , Diabetes Mellitus Experimental/enzimología , Óxido Nítrico Sintasa/metabolismo , Pentoxifilina/uso terapéutico , Testículo/efectos de los fármacos , Testículo/enzimología , Vasodilatadores/uso terapéutico , Animales , Apoptosis/efectos de los fármacos , Biopsia , Ensayo de Inmunoadsorción Enzimática , Isoenzimas/biosíntesis , Masculino , Ratas , Ratas Wistar , Túbulos Seminíferos/patología , Testosterona/metabolismo
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