雷公藤多苷对青春期大鼠睾丸组织的影响及其机制的研究
本文选题:雷公藤多苷 + 青春期大鼠 ; 参考:《宁夏医科大学》2012年硕士论文
【摘要】:目的观察雷公藤多苷对青春期大鼠睾丸组织结构及精原细胞分化、血清睾酮的影响并探讨其机制。方法青春期雄性SD大鼠(postnatal day35,PND35)48只,随机分为3组(n=16),对照组给予1%羧甲基纤维素钠6ml/(kg d)、雷公藤多苷单倍剂量组给予雷公藤多苷6mg/(kg d)、双倍剂量组给予12mg/(kg d)灌胃至性成熟早期(PND63)。停药24小时每组随机取8只,检测睾丸重量、睾丸脏器系数、生精细胞计数,光镜、电镜下观察睾丸组织学改变;用免疫组化法检测生精细胞c-kit表达;酶联免疫吸附试验测定血清睾酮浓度。剩余大鼠于停药后4周(PND92)检测上述各指标。结果停药24小时,与对照组比较,两个实验组睾丸重量、睾丸脏器系数及血清睾酮含量均无明显变化(P0.05),支持细胞及间质组织较对照组无明显变化;单倍剂量组生精细胞计数减少、c-kit表达下调(P0.05);双倍剂量组生精细胞计数较对照组明显减少,c-kit表达下调(P0.05)。停药4周,单倍剂量组睾丸重量、脏器系数、生精细胞计数、生精细胞c-kit表达及血清睾酮含量与对照组比较差别无统计学意义(P0.05),电镜下可见支持细胞萎缩;双倍剂量组睾丸重量、生精细胞计数明显下降(P0.01)、脏器系数明显降低(P0.05)、生精细胞c-kit表达下调、血清睾酮水平明显降低(P0.01),生精上皮仅可见少量精原细胞及支持细胞,支持细胞空泡样变,紧密连接分离,曲细精管萎缩,基膜迂曲、断裂,间质水肿,间质血管内皮细胞增生,血管基膜断裂,血管腔狭窄。结论1、雷公藤多苷可致青春期大鼠睾丸组织损伤,,损伤程度与剂量有关,双倍剂量所致损伤较单倍剂量明显,并可引起血清睾酮含量降低;单倍剂量雷公藤多苷所致生精细胞损伤停药后有所恢复;2、雷公藤多苷对青春期大鼠睾丸组织的损伤有迟发性;3、雷公藤多苷所致青春期大鼠睾丸组织迟发性损伤的机制包括抑制精原细胞分化、破坏血睾屏障以及影响睾丸组织血供,这些机制可能是雷公藤多苷导致青春期睾丸组织损伤的重要原因。
[Abstract]:Objective to investigate the effects of tripterygium wilfordii polyglycosides on testicular structure, spermatogonial differentiation and serum testosterone in adolescent rats.Methods Forty-eight male Sprague-Dawley rats were randomly divided into 3 groups. The control group was given 1% carboxymethyl cellulose sodium 6ml/(kg dronium, the tripterygium wilfordii polyglycoside 6mg/(kg dai group was given tripterygium wilfordii polyglycoside 6mg/(kg dung, and the double dose group was given 12mg/(kg d) until the early stage of sexual maturation.The weight of testis, testicular organ coefficient, spermatogenic cell count, histological changes of testis were observed under light microscope and electron microscope, and the expression of c-kit in spermatogenic cells was detected by immunohistochemical method.Serum testosterone concentration was determined by enzyme linked immunosorbent assay (Elisa).All the above indexes were detected by PND 92 in the remaining rats 4 weeks after withdrawal.Results there were no significant changes in testicular weight, testicular organ coefficient and serum testosterone content in the two experimental groups compared with the control group for 24 hours. The Sertoli cells and interstitial tissue had no significant change compared with the control group.The number of spermatogenic cells in the single dose group decreased significantly compared with that in the control group, and that in the double dose group was significantly lower than that in the control group.After 4 weeks of withdrawal, testicular weight, organ coefficient, spermatogenic cell count, c-kit expression and serum testosterone content of spermatogenic cells in the single dose group were not significantly different from those in the control group (P 0.05). Atrophy of Sertoli cells was observed under electron microscope.In double dose group, testicular weight, spermatogenic cell count and viscera coefficient decreased significantly, c-kit expression in spermatogenic cells decreased, serum testosterone level decreased significantly, only a few spermatogonial cells and Sertoli cells were found in spermatogenic epithelium.Vacuolar degeneration of Sertoli cells, tight junction separation, atrophy of seminiferous tubules, convoluted basal membrane, rupture of basement membrane, interstitial edema, proliferation of vascular endothelial cells, rupture of basement membrane and stenosis of blood lumen.Conclusion (1) Tripterygium wilfordii polyglycosides can cause testicular tissue injury in puberty rats, the degree of injury is related to the dose, the damage caused by double dose is more obvious than that by single dose, and the serum testosterone content can be decreased by tripterygium wilfordii.The injury of spermatogenic cells induced by tripterygium wilfordii polyglycosides at a single dose recovered 2%. The damage of tripterygium wilfordii polyglycosides to testis of pubertal rats was delayed, and that of tripterygium wilfordii polyglycosides was delayed injury in testis of pubertal rats.Mechanisms include inhibition of spermatogonia differentiation,The destruction of the blood-testis barrier and the influence of the blood supply of testis may be the important causes of the injury of testicular tissue caused by tripterygium wilfordii polyglycosides.
【学位授予单位】:宁夏医科大学
【学位级别】:硕士
【学位授予年份】:2012
【分类号】:R285.5;R726.9
【参考文献】
相关期刊论文 前10条
1 杨建一;高宝珍;李莉;王文娟;郭红刚;边思成;;雷公藤多甙对雄性小鼠生殖细胞毒性的研究[J];癌变.畸变.突变;2008年05期
2 骆永伟;施畅;吴纯启;胡中慧;杨保华;王全军;张玉杰;廖明阳;;抗肿瘤化合物MC004对雄性大鼠生殖毒性的研究[J];癌变.畸变.突变;2009年03期
3 崔毓桂;傅广波;张桂元;钱立新;狄福松;;男性不同发育阶段靶组织中雄激素水平生理性变化[J];国际生殖健康/计划生育杂志;2009年01期
4 潘艳琳;林丽芳;于静;;雷公藤不良反应75例分析[J];海峡药学;2011年08期
5 王景会;刘霞;;雷公藤多苷治疗过敏性紫癜临床研究[J];中医学报;2011年04期
6 苏桂花;苑述刚;马少丹;张英杰;阮时宝;;雷公藤的本草学及临床应用研究[J];河南中医;2011年04期
7 江云鸥;陈倩岚;张志勇;;雷公藤多苷片不良反应的回顾性分析[J];华西医学;2009年09期
8 贾太和 ,孙辉臣 ,王晓旭 ,康尔竹 ,董志英 ,修贺明 ,张春然 ,张荣莲 ,徐铮;雷公藤糖浆对人精子发生的影响[J];中国计划生育学杂志;1994年03期
9 张健,李健,王晓云,孙烨,牛丽静,段相林;大鼠生精小管体视学及PCNA、凋亡表达的发育变化研究[J];解剖学报;2002年06期
10 石之虎;廖晓岗;李庆春;邹聪;;镉对培养大鼠睾丸支持细胞的损伤及黄芪的拮抗作用[J];解剖学杂志;2008年06期
本文编号:1767495
本文链接:https://www.wllwen.com/yixuelunwen/eklw/1767495.html