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目的观察锌对乙醇长期摄入所致大鼠睾丸损伤的保护作用机制。方法30只健康雄性成年SD大鼠随机分为对照组、乙醇组、乙醇+葡萄糖酸锌组,各组每日分别灌胃0,7.5g/kg乙醇、7.5g/kg乙醇+7.7mg/kg葡萄糖酸锌,连续13周后检测精子计数、活动率、精子畸形率,血清睾酮;光、电镜观察睾丸的形态改变,同时测定睾丸线粒体中丙二醛(MDA)的产生量,免疫组织化学法和蛋白印迹(western-blot)检测睾丸组织中诱导型一氧化氮合酶(iNOS)的表达。结果与对照组(38.0±7.9)×106/mL比较,乙醇组精子计数为(8.2±5.1)×106/mL,减少了78%(P<0.05),精子活动率下降了71%(P<0.05),精子畸形率明显升高(P<0.05),血清睾酮水平明显降低(P<0.05);睾丸生精上皮结构破坏,支持细胞和各级生精细胞均有退化变性;睾丸生精细胞iNOS表达明显增强(P<0.05);睾丸线粒体丙二醛含量明显升高。乙醇+葡萄糖酸锌组较单纯乙醇组精子计数、精子活动率上升,生精细胞退化变性程度减轻,睾丸生精细胞iNOS表达减弱(P<0.05),睾丸线粒体MDA减少,但血清睾酮仍低于对照组。结论长期摄入乙醇会抑制精子生成和睾酮合成,补充锌可以抑制乙醇引起的睾丸过氧化损伤,保护睾丸的生精功能。
Objective To observe the protective mechanism of zinc on testicular damage induced by long-term ethanol ingestion in rats. Methods Thirty healthy adult male Sprague-Dawley rats were randomly divided into control group, ethanol group and ethanol + zinc gluconate group. The rats in each group were orally administered with 0, 7.5g / kg ethanol, 7.5g / kg ethanol + 7.7mg / kg Zinc gluconate, and the sperm count, activity rate, sperm deformity rate and serum testosterone were measured after 13 weeks of continuous operation. Morphological changes of testis were observed under light and electron microscopes, and the amount of malondialdehyde (MDA) in testis mitochondria was measured. Immunohistochemistry And western blot were used to detect the expression of inducible nitric oxide synthase (iNOS) in testis. Results Compared with the control group (38.0 ± 7.9) × 106 / mL, the sperm count in ethanol group was (8.2 ± 5.1) × 106 / mL, decreased by 78% (P <0.05) and sperm motility decreased by 71% 0.05), the sperm deformity rate increased significantly (P <0.05), the level of serum testosterone decreased significantly (P <0.05); the structure of testicular germinal epithelium was destroyed, the supporting cells and spermatogenic cells at all levels degenerated; iNOS expression was significantly increased (P <0.05); testicular mitochondrial MDA content was significantly increased. Compared with simple alcohol group, the sperm motility of ethanol + zinc gluconate group increased, the degree of degeneration of spermatogenic cells decreased, the expression of iNOS decreased (P <0.05) and the content of testicular mitochondrial MDA decreased Control group. Conclusion Long-term intake of ethanol inhibits spermatogenesis and testosterone synthesis, and zinc supplementation can inhibit the testicular peroxide damage induced by ethanol and protect the spermatogenic function of testes.