苦杏仁苷对醋酸铅所致雄性小鼠生精障碍的影响

Effect of amygdalin on the spermatogenesis disturbance induced by lead acetate in male mice

目的研究苦杏仁苷(amygdalin)对醋酸铅所致雄性小鼠生精障碍的影响,并探讨其作用机制。方法采用腹腔注射醋酸铅(20 mg/kg)连续7 d建立雄性小鼠生精障碍模型,造模第2天始,苦杏仁苷低、中、高剂量组分别腹腔注射苦杏仁苷(15、30和60 mg/kg),连续42 d。观察雄性小鼠的精子密度、精子畸变率变化,检测血清中睾酮(testosterone,T)的含量及睾丸组织匀浆的乳酸脱氢酶(lactic dehydrogenase,LDH)、山梨醇脱氢酶(sorbitol dehydrogenase,SDH)、Na^+-K^+-ATP酶、Mg^(2+)-ATP酶、超氧化物歧化酶(superoxide dismutase,SOD)、一氧化氮(nitric oxide,NO)、肿瘤坏死因子α(tumor necrosis factorα,TNF-α)水平的变化,并观察睾丸组织的病理改变。结果与模型组比较,苦杏仁苷各剂量组的精子密度增高、精子畸变率降低,苦杏仁苷各剂量组睾丸组织中LDH、SDH、Mg^(2+)-ATP酶的活性增高,苦杏仁苷中、高剂量组睾丸组织中Na^+-K^+-ATP酶、SOD活性增强、NO及TNF-α含量降低、血清中T含量增高,同模型组比较差异有统计学意义(P<0.05或P<0.01)。模型组睾丸组织生精上皮明显变薄,生精细胞层次和数量减少,多数生精小管腔见少量精子形成,而苦杏仁苷中、高剂量可改善醋酸铅所致的睾丸组织损伤。结论苦杏仁苷对醋酸铅所致小鼠生精障碍的有一定改善作用,机制可能是通过抗氧化、降低NO水平,从而能稳定细胞膜、增强精子生成中能量代谢酶活性及抑制炎症介质。

Objective To study the effect of amygdalin and its mechanism for spermatogenesis obstruction caused by lead acetate in male mice. Methods The spermatogenesis obstruction of male mice model was built by ip injection with lead acetate（ 20 mg / kg） for 7 d,the 2 d model made mice in low,medium and gigh doses amygdalin were treated by amygdalin,respectively（ 15,30,60 mg / kg） by ip injection for 42 d. The mice were sacrificed on 43 d for the measurement of the sperm density,the sperm aberration rate. The content of testosterone（ T） in blood serum,the levels of lactate dehydrogenase（ LDH）,sorbitol dehydrogenase（ SDH）,Na~＋-K~＋-ATPase,Mg^（2＋）-ATPase,superoxide dismutase（ SOD）,nitric oxide（ NO） and tumor necrosis factor α（ TNF-α） in testicular tissue homogenate were assayed respectively. The pathological changes of testicular tissues were observed. Results Compared with the model group,sperm density was increased,the sperm aberration rate mice was dereased,the activities of LDH,SDH,Mg^（2＋）-ATPase in testicular tissue homogenate were improved in different doses amygdalin groups. The activities of Na~＋-K~＋-ATPase and and SOD in testicular tissue homogenate and the content of T in blood serum were increased,the contents of NO and TNF-α in testicular tissue homogenate were decreased in medium and high dose groups. Pathological change of testis showed there were decline of spermatogenic cells in levels and numbers and few spermiogenesis in most of seminiferous tubule in model group. Those change above could be reversed by amygdalin. Conclusion Amygdalin had certain improvement on spermatogenesis obstruction of mice caused by lead acetate,its mechanism may be related to anti-oxidation and decreasing NO,then stabilizing cell membrane,enhancing enzymatic activity of energy metabolism and inhibiting inflammatory mediator.