基于氧化应激分子效应探讨益肾活血法对大鼠精子活动力的调控作用机制

Low sperm motility disease is harmful to human reproductive health，The complexity of the pathogenesis and the clinical curative effect unsatisfied. It's difficulties for clinical diagnosis and treatment even many patients without symptoms and signs. It has been find the mechanism of oxidative stress in male infertility especially in low sperm motility disorder plays an important role By some research. Related prescriptions research is around the mechanism of action of nitric oxide and superoxide dismutase. It has found that sperm motility can be improved by tonifying kidney and promoting blood circulation in the preliminary study and clinical practice, But lack of study on molecular mechanism of verification. The proposed hypothesis as whether the tonifying kidney and promoting blood circulation is the key to improve sperm function by oxidative stress pathway. The cellular oxidative stress mechanism could be activated by using YiShenHuoXue Decoction to improve sperm motility. Based on this, low sperm motility rats has been chosen as research object. And nitric oxide, superoxide dismutase, antioxidant enzyme system and intracellular oxidative stress have being the starting point to study the intracellular mechanism of sperm motility improving by YiShenHuoXue Decoction. It provide a scientific basis for prevention and treatment of sperm motility disorder when explore the microscopic mechanism of sperm motility improving by tonifying kidney and promoting blood circulation from the molecular level.

精子活力低下症是危害人类生殖健康的主要因素，其发病机理复杂，临床疗效不满意。甚则许多患者无症状体征表现，给临床诊治带来了困难。研究发现，氧化应激机制在男性不育症尤其是精子活力低下症中起着重要的作用。相关方药的研究也围绕着对一氧化氮、超氧化物歧化酶作用机制进行。前期研究及临床实践积累，发现通过益肾活血法，用益肾活血方能够改善精子活动力，但缺乏分子机制研究验证。据此提出假说：是否氧化应激途径是益肾活血法改善精子活动力的关键。用益肾活血方改善精子活动力，机体细胞的氧化应激机制可能被激活。基于此，通过实验性精子活力低下症大鼠作为研究对象，用一氧化氮、超氧化物歧化酶等抗氧化酶系统及细胞内氧化应激作为切入点，研究益肾活血方改善精子活动力的细胞内机制。旨在从分子层面探索益肾活血法改善精子活力的微观机制，为临床防治精子活力低下提供科学的依据。

精子活力低下症是危害人类生殖健康的主要因素，其发病机理复杂，临床疗效不满意。甚则许多患者无症状体征表现，给临床诊治带来了困难。研究发现，氧化应激机制在男性不育症尤其是精子活力低下症中起着重要的作用。相关方药的研究也围绕着对一氧化氮、超氧化物歧化酶作用机制进行。前期研究及临床实践积累，发现通过益肾活血法，用益肾活血方能够改善精子活动力，但缺乏分子机制研究验证。据此提出假说：是否氧化应激途径是益肾活血法改善精子活动力的关键。用益肾活血方改善精子活动力，机体细胞的氧化应激机制可能被激活。基于此，通过实验性精子活力低下症大鼠作为研究对象，用一氧化氮、超氧化物歧化酶等抗氧化酶系统及细胞内氧化应激作为切入点，研究益肾活血方改善精子活动力的细胞内机制。本研究明确了益肾活血方可以一定程度上改善大鼠睾丸精子的活动力，揭示出了益肾活血方改善精子活动力的细胞内氧化应激机制。益肾活血方可能通过降低MDA、NO含量，上调病理模型大鼠睾丸中的GSH-PX含量及GSH表达，增加大鼠睾丸GR基因表达，增强UCP2表达，降低P38的表达以及抑制其磷酸化，降低ERK的表达以及抑制其磷酸化，降低大鼠睾丸FAS及FASL表达，增加大鼠睾丸组织中的PKC表达的途径增加其抗氧化损伤能力，从而提高大鼠睾丸精子活动力。 进而从分子层面揭示了益肾活血法改善精子活力的微观机制，为临床防治精子活力低下提供了科学的依据。