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作 者:李杜娟[1] 王家富[1] 黄庆玉[1] 刘伟[1] 房建强[1] 王振军[1]
机构地区:[1]泰山医学院病理学教研室,山东泰安271000
出 处:《泰山医学院学报》2005年第3期196-199,共4页Journal of Taishan Medical College
摘 要:目的观察维生素E对环磷酰胺致小鼠睾丸损伤的拮抗作用,并探讨其相关机制。方法随机将小鼠分成3组:正常对照组、CP对照组、维生素E治疗组。CP对照组和维生素E治疗组小鼠经口灌胃5 mg/kg.d-1CP,维生素E治疗组小鼠每天给予CP处理后4 h,皮下注射50 mg/kg.d-1维生素E;正常对照组小鼠经口灌胃等量生理盐水。各组均连续处理28天。观察血清FSH、LH、T水平,睾丸组织SOD、GSHPx、CAT的活性及MDA量,睾丸重量系数,睾丸组织结构。结果与CP对照组相比,维生素E治疗组血清FSH、LH、T水平显著升高,自由基清除酶SOD、GSHPx、CAT活性明显提高,脂质过氧化产物MDA量显著下降,睾丸重量系数增加,生精功能恢复。结论维生素E可有效拮抗环磷酰胺的睾丸毒副作用,其作用机制可能与维生素E清除氧自由基、抗氧化作用及其促进垂体前叶促性腺激素的释放等有关。Objective: To observe the antagonistic action of vitamin E on testis injury induced by cyclophosphamide, and study the eorrdative mechanisms. Methods: Twenty four sexually mature male mice were divided randomly into three groups: the contrast control group, the cyclophosphamide treatment group, the cyclophosphamide and vitamin E co-administered group. The latter two groups were given cyclophosphamide by gavage at a dose of 5 mg/kg body weight/day. The cyclophosphamide and vitamin E co-administered group was given vitamin E by subcutaneous injection at a dose of 50 mg/kg body weight/day after 4 h of cyclophosphamide treatment. The contrast control group was gavaged with equivalent water. The treatment period for all groups was 28 days. The level of plasma FSH, LH, T and the activity of testicular SOD, GSHPx, CAT and the level of testicular MDA were detected. The testieular somatic indexs were measured. The histological sections of testis were examined by light microscope. Results: As compared with the cyclophosphamide treatment group in cyclophosphamide and vitamin E co-administered group, The histological structure of testis recovered significantly, and MDA level was significantly diminished, while the plasma level of FSH, LH, T and the activity of testicular SOD, GSHPx, CAT were increased. Conclusion: Vitamin E has a protective effect on cyclophosphamide-induced testicular injury. The possible mechanism may be its seavenging free radical action and antioxidant effect, as well as its some stimulatory effects on gonadotrophin releasing of pituitary anterior lobe.
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