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目的观察雄性大鼠慢性感染弓形虫后血清及睾丸局部促黄体生成素(LH)、睾酮(T)水平及其受体的动态变化,探讨弓形虫感染对大鼠生精细胞损伤及生精过程的影响。方法选用9~10周龄雄性SD大鼠88只,随机分为对照组和弓形虫感染组。弓形虫感染组大鼠腹腔注射1×104个速殖子/只。对照组注射等量生理盐水。于感染前和感染后第3、6、9、12、……和30d两组各取4只大鼠,采用放射免疫法检测大鼠血清LH、T以及睾丸局部T水平的动态变化,采用免疫组化sABC法检测睾丸LH受体(LHR)和T受体(AR)的变化,并对睾丸组织进行病理学观察。结果整个实验期内弓形虫感染组大鼠血清LH[(29.3±3.3)mIU/ml]与对照组[(25.5±2.75)mIU/ml]差异无统计学意义(P>0.05);感染组大鼠T水平尤其是睾丸局部T水平在急性期[(238.3±38.9)ng/dl]较对照组[(915.4±119.3)ng/dl]显著下降(P<0.01),之后血清T逐渐升高,实验末期恢复至对照组水平(P>0.05),睾丸局部T仍维持低水平(P<0.01)。感染组大鼠的睾丸间质细胞(leydig cell)LHR及AR表达均增强,精母细胞及支持细胞AR表达增强。病理学检查感染组大鼠生精小管细胞层次混乱,精子细胞及精子减少甚至管腔关闭,至实验末期生精过程未见明显改善。结论雄性大鼠感染弓形虫后导致T水平尤其是睾丸局部T水平迅速降低,睾丸LHR及AR表达增强,导致生精细胞损伤和生精过程阻滞于精母细胞期。
Objective To observe the local luteinizing hormone (LH), testosterone (T) levels and their receptors in serum and testis of chronic infection with Toxoplasma gondii in male rats, and to explore the effects of Toxoplasma gondii infection on spermatogenic cell damage and spermatogenesis in rats Impact. Methods Eighty-eight male SD rats aged 9-10 weeks were randomly divided into control group and Toxoplasma gondii infection group. Toxoplasma gondii infection rats were intraperitoneal injection of 1 × 104 tachyzoites / only. The control group was injected with normal saline. Before and 3, 6, 9, 12, ... and 30 d after infection, 4 rats in each group were taken, and the changes of serum LH and T and the local T level in testis were detected by radioimmunoassay. Tissue sABC method was used to detect the changes of testicular LH receptor and T receptor (AR), and pathological changes of testis were observed. Results There was no significant difference in LH (29.3 ± 3.3) mIU / ml between Toxoplasma gondii infection group and control group [(25.5 ± 2.75) mIU / ml] (P> 0.05) The level of T and especially the level of T in testis decreased significantly in the acute phase [(238.3 ± 38.9) ng / dl vs [(915.4 ± 119.3) ng / dl) (P <0.01) At the end of experiment, the level of T in testis remained low (P <0.01). In the infected group, the expression of LHR and AR increased in leydig cells and the expression of AR in spermatocytes and supporting cells increased. In the pathological examination, the seminiferous tubules of rats in the infection group were confused, the sperm cells and sperm were reduced or even the lumen was closed, and no significant improvement was observed in the spermatogenic process at the end of the experiment. Conclusion Toxoplasma gondii infection in male rats resulted in the rapid decrease of T level, especially the local T level in testis. The expression of LHR and AR in testis increased, resulting in spermatogenic cell injury and spermatogenesis blocked in spermatocyte stage.