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目的:研究苦参总黄酮(flavonoids from Sophora flavescens)对醋酸铅诱导雄性小鼠睾丸损伤的影响及其机制。方法:昆明小鼠分为4组:正常对照组、模型组、苦参总黄酮组及HCG组,采用醋酸铅(40 mg/kg)连续灌胃7d建立雄性小鼠睾丸损伤模型,造模第2天始,苦参总黄酮组灌胃苦参总黄酮600 mg/kg,HCG组腹腔注射HCG 500IU/kg,连续30 d。观察雄性小鼠的精子活力、精子畸形率;睾丸组织匀浆检测超氧化物歧化酶(SOD)、一氧化氮合酶(NOS)、一氧化氮(NO)等指标;并观察睾丸组织的病理改变。结果:与正常对照组比较,模型组精子活力显著降低,精子畸形率增高,睾丸组织中SOD和NOS的活性降低、NO含量减少(P<0.05或P<0.01),模型组睾丸组织病理表现生精上皮显著变薄,生精细胞层次和数量均减少,生精小管腔可见少量精子形成。与模型组比较,苦参总黄酮组的精子活力相应增高,精子畸形率降低,睾丸组织中SOD、NOS的活性增高、NO含量增加(P<0.05或P<0.01),因醋酸铅所致的睾丸组织损伤明显改善。结论:苦参总黄酮对醋酸铅所致雄性小鼠睾丸损伤有一定保护作用,作用机制可能与抗氧化及影响NOS-NO系统有关。
Objective: To study the effect and mechanism of flavonoids from Sophora flavescens on testicular injury induced by lead acetate in male mice. Methods: Kunming mice were divided into 4 groups: normal control group, model group, total flavonoids of Sophora flavescens group and HCG group. The testis injury model was established by continuous administration of lead acetate (40 mg / kg) The beginning of the day, Sophora flavescens total flavonoids flavonoids gavage 600 mg / kg, HCG group intraperitoneal HCI 500IU / kg for 30 d. The sperm motility and sperm deformity of male mice were observed. The contents of superoxide dismutase (SOD), nitric oxide synthase (NOS) and nitric oxide (NO) in testis homogenate were measured. The pathological changes of testis change. Results: Compared with the normal control group, the sperm motility, the sperm deformity rate, the activity of SOD and NOS in the testis decreased and the content of NO decreased (P <0.05 or P <0.01) Significant thinning of fine epithelium, spermatogenic cell layers and the number are reduced, small spermatozoon visible sperm formation. Compared with the model group, the total flavonoids in Sophora flavescens group increased sperm motility, decreased the sperm deformity rate, increased the activity of SOD and NOS in testis tissue, and increased the content of NO (P <0.05 or P <0.01) Tissue damage significantly improved. Conclusion: Total Flavonoids of Sophora flavescens Ait has a protective effect on the testicular damage induced by lead acetate in male mice. The mechanism may be related to the antioxidation and NOS-NO system.