论文部分内容阅读
目的研究弓形虫感染雄性大鼠后引起的Th1/Th2细胞因子漂移对黄体生成素(LH)、睾酮(T)水平的影响,探讨其对雄性生精细胞损伤的通路。方法选用9~10周龄雄性SD大鼠18只,随机分为健康对照组和弓形虫感染组。弓形虫感染组分为低剂量组和高剂量组2组,分别感染1×103和1×104个速殖子/只(采用腹腔注射法)。感染后第7 d,ELISA检测血清IFN-γI、L-4及NO水平,放射免疫法检测大鼠血清LH、T以及睾丸局部T水平,并对睾丸组织进行病理学观察。结果感染弓形虫雄性大鼠血清IFN-γ与NO水平较健康对照鼠显著升高(P<0.01),IL-4有一定程度升高,但IFN-γ/IL-4比值显著变大(P<0.01);血清及睾丸局部LH水平无显著变化;T水平尤其是睾丸局部T水平显著降低(P<0.01)。病理学检查感染组大鼠生精小管细胞层次混乱,初级精母细胞、次级精母细胞显著减少,管腔内精子稀少甚至管腔关闭。结论雄性大鼠感染弓形虫后,可能是由Th1细胞因子极化作为始动因素介导激素分泌异常,尤其是睾丸局部睾酮水平迅速降低,并进一步诱导生精细胞损伤和生精停滞。
Objective To study the effects of Th1 / Th2 cytokine drift on the levels of LH and testosterone (T) induced by Toxoplasma gondii Infection in male rats, and to explore the pathways leading to the injury of male spermatogenic cells. Methods Eighteen male Sprague-Dawley rats aged 9-10 weeks were randomly divided into healthy control group and Toxoplasma gondii infection group. Toxoplasma infection was divided into two groups: low dose group and high dose group, which were infected with 1 × 103 and 1 × 104 tachyzoites / peritoneal injection respectively. Serum levels of IFN-γI, L-4 and NO were detected by ELISA 7 days after infection. Serum LH, T and T testicular tissue were detected by radioimmunoassay. Pathological examination of testis was also performed. Results Serum levels of IFN-γ and NO in male rats with Toxoplasma gondii were significantly higher than those in healthy controls (P <0.01), IL-4 was increased to a certain extent, but the ratio of IFN-γ / IL-4 was significantly increased <0.01). Serum and testicular local LH levels did not change significantly; T level, especially testicular local T level was significantly decreased (P <0.01). Pathological examination of infected rat group of seminiferous tubule cells confusion, primary spermatocytes, secondary spermatocytes significantly reduced intraluminal sperm sparse or even close the lumen. Conclusion After Toxoplasma gondii infection in male rats, the abnormal secretion of hormones may be mediated by Th1 cytokine polarization, especially the rapid decrease of testosterone levels in testis and further induce the spermatogenic cell damage and spermatogenic arrest.