实验性精索青岛脉曲张对生精上皮细胞间连接的影响

Experimental varicoceles were created in adult male Wistar rats by partially occluding the left renal vein. The affect of the varicocele on ipsilateral testis was studied at intervals over 15 weeks via ultrathin sections and freeze-etching replica technique examined under electron microscope. Observations showed that varicocele resulted in injuries of Sertoli-Sertoli cell and Sertoli cell-spermatid junctional complexes. Abnormal changes of Sertoli cell-spermatid junctional complexes might lead to spermiogenic arrest and spermatids slough, while those of Sertoli-Sertoli cell junctional complexes to dysfunction of barrier and abnormal alteration of microenvironment of seminiferous tubule. Probably, this is one of the reasons that the fertility was not improved in some patients even after high level ligation of the internal spermatic vein.     

GSPE对精索扭转损伤大鼠睾丸组织结构、生精细胞的影响研究

目的 探究GSPE对精索扭转损伤大鼠睾丸组织结构、生精细胞的影响.方法 把实验大鼠平均分为3组,sham组、TT组和GSPE组.测定三组大鼠氧化应激指标,包括SOD活性和MDA含量;测量大鼠睾丸质量和Johnsen评分;观察睾丸组织形态结构的改变及生精细胞的凋亡指数;免疫组化检测睾丸组织中Bax和Bcl-2的表达.结果...     

精索静脉曲张大鼠睾丸生精功能的定量研究

目的: 探索精索静脉曲张睾丸病理改变的定量指标。方法: 选择30例SD大鼠, 20例作为手术组, 建立曲张模型; 10例作为假手术对照组, 取下睾丸常规染色切片, 用Makler积分法分别测量手术组200个, 对照组100个曲细精管内径、管周膜厚度、细胞层数及生精细胞成熟程度, 并计算平均得分。结果: 精索静脉曲张组的曲细精管内径显著缩小, 管周膜增厚, 细胞层次减少, 生殖细胞成熟障碍, Makler评分显著低于假手术组。结论: Makler评分能对静脉曲张所致的睾丸病理损害作出客观的评价, 值得在不育症研究中推广。     

实验性精索静脉曲张诱导青春期大鼠附睾细胞凋亡的研究

目的：研究实验性精索静脉曲张（EVC）大鼠附睾细胞凋亡及其显微、超微结构的变化。 方法： 采用青春期雄性Wistar大鼠复制左精索静脉曲张模型，以末端脱氧核糖核酸转移酶介导的dUTP缺口末端标记法（TUNEL）检测细胞凋亡,常规制作附睾体部光镜、电镜标本，观察附睾组织细胞形态变化。 结果： 实验组（VG）细胞凋亡率显著高于假手术组（SOG）（P<0.01），实验组左、右侧细胞凋亡率有差别，但无显著意义（P>0.05）。光镜下主要改变有附睾管萎缩，上皮细胞出现空泡化，上皮内晕、亮细胞数明显增多。电镜下主要表现为主细胞内溶酶体增多、变大，残余小体增加，内质网扩张，线粒体嵴模糊，高尔基复合体空泡化；核染色质致密，形成大小不等的团块，边集于核膜处；上皮细胞游离面微绒毛稀少，可见局灶性断裂和破坏。 结论： 青春期大鼠实验性精索静脉曲张可致附睾组织细胞凋亡过度，使其显微及超微结构明显改变，这些变化可能是影响精索静脉曲张患者生育能力的机制之一。     

睾丸波形蛋白表达与生精细胞凋亡的关系

睾丸的生精上皮具有高度增殖能力,生精过程中细胞增殖与凋亡的动态平衡,对于维持精子的生成的数量和质量具有重要的作用。外来化学毒物可以直接引起睾丸损伤,导致生精细胞过量凋亡,从而导致精子生成减少。生精细胞凋亡时细胞骨架蛋白改变的研究成为一个热点,睾丸波形蛋白表达发生了异常改变,但睾丸波形蛋白表达与生精细胞凋亡的相关性还需进一步研究。     

凋亡生精细胞的观察

用瑞－姬法观察凋亡生精细胞的各种形态，即凋亡的初级精母细胞、次级精母细胞、精子细胞，并观察了凋亡的前列腺上皮细胞的形态，就生精细胞凋亡原因进行了分析。     

细胞色素C和波形蛋白在染锰大鼠睾丸表达及对精子发生的抑制作用

目的研究氯化锰对大鼠生精细胞细胞色素C(cyto-c)和支持细胞波形蛋白(VM)表达的影响及对生精功能的抑制效应。方法雄性SD大鼠随机分为空白对照组,低剂量(15 mg/kg Mn Cl2)和高剂量(30 mg/kg Mn Cl2)组,8只/组。Mn Cl2组分别染锰4周和6周,空白对照组给予等容生理盐水,给药途径均为腹腔注射,取睾丸免疫组织化学(SABC)法检测生精细胞cyto-c和VM表达,测定睾丸脏器系数,取附睾检测精子数量和精子畸形率。结果与空白对照组比较,各染锰组生精细胞cyto-c阳性细胞率和支持细胞VM阳性细胞率及各生精功能指标均显著降低,并呈一定的时间-效应关系和剂量-效应关系。各组大鼠精子数量与cyto-c阳性细胞率和VM阳性细胞率均呈正相关。结论锰可诱导大鼠生精细胞cyto-c和支持细胞VM表达,抑制生精细胞增殖,产生生殖毒性效应。     

SB203580对大鼠隐睾生精细胞凋亡的影响

目的:探讨SB203580对大鼠隐睾所致生精细胞凋亡过程中的作用。方法:雄性SD大鼠随机分为隐睾组、隐睾 SB203580(p38MAPK抑制剂)组、隐睾 溶媒组、假手术组。复制单侧隐睾模型,术后分别腹腔内注射溶媒或SB203580。7 d后快速断颈椎处死,TUNEL原位末端标记法结合流式细胞术(FCM)检测各组右侧睾丸生精细胞凋亡,免疫组化观察各组右侧睾丸磷酸化p38MAPK蛋白表达的变化。结果:FCM及TUNEL法均显示隐睾 SB203580组生精细胞凋亡指数低于隐睾组和隐睾 溶媒组,同时磷酸化p38MAPK蛋白表达减少。结论:SB203580能降低p-p38MAPK蛋白表达并抑制热压诱导的生精细胞凋亡。     

生精细胞凋亡及其调控

在细胞生物学领域,细胞凋亡的实现调控着细胞死亡和增殖的平衡,故具有重要的生物学意义。生精细胞的凋亡在生精过程中具有极其重要的作用。近年来,睾丸内细胞凋亡的研究在国内外已成为热点之一。本文将就生精细胞凋亡的的阶段性、生理意义、形态特点、激素调节、基因调控等诸多方面的研究概况作一综述。     

生精细胞的凋亡与调控

生精细胞凋亡是近年来生殖生物学的研究热点之一 ,动物的不同发育阶段 ,年龄差异 ,激素水平尤其FSH是影响生精细胞凋亡的重要因素。本文重点对生精细胞凋亡的影响因素及其基因调控机制进行综述。     

高糖对人肾系膜细胞GSH-PX和PDGF-B表达影响及茶多酚干预作用

目的探讨高糖条件下系膜细胞氧化失衡与血小板源性生长因子—B（PDGF—B）表达之间的关系,通过抗氧化剂茶多酚证实氧化应激在早期糖尿病中的作用。方法将培养的系膜细胞分为正常对照组、高糖组、茶多酚对照组和茶多酚干预组,分别在0、12、24、36、48h采用分光光度法检测上清液还原型谷胱甘肽过氧化物酶（GSH—PX）活性,以及免疫细胞化学法和RT—PCR法检测0、12、36h的PDGF—B mRNA和蛋白的表达情况。结果①高糖条件下GSH—PX活性下降,抗氧化能力下降,氧化失平衡;茶多酚可增加抗氧化酶GSH—PX的活性。②高糖组系膜细胞PDGF—B mRNA和蛋白的表达比正常对照组均增加（P〈0．05）;茶多酚干预组比高糖组有明显下降（P〈0．05）。结论高糖能促进系膜细胞活性氧和PDGF—B的表达增加,茶多酚可抑制该作用。     

Effect of tea polyphenols on histamine release from rat basophilic leukemia (RBL-2H3) cells: the structure–inhibitory activity relationship

We studied the effect of tea polyphenols on histamine release from rat basophilic leukemia (RBL-2H3) cells. Among tea polyphenols, (-)-epigallocatechin gallate (EGCG) most strongly and dose-dependently inhibited histamine release from cells stimulated with a calcium ionophore, A23187. (-)-Epigallocatechin (EGC) and (-)-epicatechin gallate (ECG) with a triphenol residue moderately inhibited histamine release, whereas diphenolic (+)-catechin (C) and (-)-epicatechin (EC) did not. The magnitude of the inhibitory effect was in the order EGCG > ECG > EGC. Among simple polyphenols, the triphenol compounds, pyrogallol (PG) and gallic acid (GA) exerted inhibitory activity, but the diphenols, pyrocatechol, hydroquinone, and resorcinol did not. In addition, the mixture of PG and GA inhibited histamine release as strongly as EGCG with two triphenol residues. Similarly, they inhibited histamine release induced by IgE-antigen complex stimulation more efficiently than that induced by A23187 stimulation. EGCG did not inhibit the increase of intracellular Ca²⁺ in RBL-2H3 cells stimulated with A23187 or IgE antigen. These results indicate that the triphenol structure plays an important role in the inhibitory activity of tea polyphenols. Their activity seemed to be exerted through the metabolic events occurring after the elevation of intracellular Ca²⁺ concentration.     

谷胱甘肽对染锰大鼠生精细胞凋亡与增殖的影响

目的:研究谷胱甘肽(GSH)对染锰大鼠生精细胞凋亡与增殖的作用及机制。方法:雄性SD大鼠48只随机分为6组,各组给锰途径为腹腔注射。采用TUNEL法检测生精细胞凋亡指数(AI);免疫组织化学法检测生精细胞增殖细胞核抗原(PCNA)表达。结果:与空白对照组比较,GSH对照组和15mg/kg GSH组生精细胞AI与生精细胞PCNA增殖指数(PI)均无显著性差异;与各自对应的单纯染锰组比较,15mg/kg GSH组和30mg/kg GSH组生精细胞AI均显著降低而PI均显著升高;30mg/kg组与15mg/kg组比较,生精细胞AI显著升高而PI显著降低;各组大鼠生精细胞AI和PI呈负相关。结论:15mg/kg和30mg/kg氯化锰可诱发大鼠睾丸生精细胞凋亡,两者存在剂量-效应关系;各组大鼠睾丸生精细胞AI和PI呈显著负相关;GSH对锰诱发大鼠生精细胞凋亡具有拮抗作用;GSH可能拮抗锰对大鼠生精细胞增殖的抑制作用。     

The peritubular myoid cells in the testes from men with varicocele: an ultrastructural, immunohistochemical and quantitative study

Ultrastructural and some immunophenotypic features of the peritubular myoid cells of testes from normal men and from men with varicocele were studied. The seminiferous tubules were classified into five types (a-e), related to the progressive degree of sclerosis measured as thickening of the lamina propria. In normal testes only type a and b tubules were found, whereas the testes from men with varicocele showed type b-e tubules. Myoid cells in tubule types a and b showed slender cytoplasmic projections with abundant, parallel arranged microfilament bundles and electron-dense bodies. In c tubules, the myoid cells showed the same ultrastructure. The myoid cells of tubules with advanced (type d) or complete (type e) sclerosis showed irregularly outlined nuclei, scant microfilament bundles and absence of electron-dense bodies. Immunostaining of myoid cells with anti-actin antibodies was intense in types a-c tubules and scant in types d and e. Immunostaining with anti-desmin antibodies was intense in tubules types a-d, but the immunoreactive cells in types c and d tubules were irregularly shaped and distributed and were scanty in tubule type e. Immunostaining with anti-vimentin antibodies was weak in types a-c tubules and intense in types d and e tubules. Quantitative studies revealed that, with the progression of sclerosis, the numbers of both actin- and desmin-immunoreactive cells per cross-sectioned tubule, and the surface area occupied by the immunostained portion of these cells, decreases while the number of vimentin-immunoreactive cells and their immunostained surface area increases.     

衰老大鼠睾丸生精细胞增殖凋亡及相关因素的变化

目的:观察衰老大鼠睾丸生精细胞增殖、凋亡及相关因素的变化。方法:D-半乳糖连续腹腔注射制作亚急性衰老的大鼠模型。SP免疫组织化学法观察睾丸生精细胞衰老过程中增殖细胞核抗原(PCNA)和端粒酶的表达,TUNEL法观察生精细胞的凋亡,原位杂交、Western印迹分析观察生精细胞p53基因的表达。结果:与正常大鼠相比,衰老大鼠睾丸PCNA阳性细胞率显著下降,端粒酶阳性细胞数明显减少,凋亡管数和凋亡阳性细胞率显著升高,p53 mRNA阳性细胞率和p53蛋白含量均有所升高。结论:衰老大鼠睾丸生精细胞增殖能力下降、凋亡增多,睾丸机能减退。     

绿茶多酚通过抑制TLR4通路减轻蛛网膜下腔出血大鼠早期脑损伤

目的 探讨绿茶多酚通过抑制TLR4通路对蛛网膜下腔出血大鼠早期脑损伤的影响.方法 建立大鼠蛛网膜下腔出血模型,随机分为模型组、绿茶多酚组、TAK-242(TLR4抑制剂)组、绿茶多酚+TAK-242组,每组12只;另取12只大鼠设为假手术组.药物处理后,对所有大鼠进行神经功能缺损评分,检测各组大鼠脑组织含水量,采用Ev...     

茶多酚的表遗传机制与肿瘤防治

茶多酚(tea polyphenols,TP)是绿茶中对人体有益的主要成分,其对多种不同类型的肿瘤发生可能具有防护作用,其中包括表遗传途径.表遗传指不改变DNA序列的情况下基因表达发生可遗传改变的机制,主要包括DNA甲基化、组蛋白修饰、染色质重塑、siRNA和miRNA调控等,在人类的大多数肿瘤中都观察到表修饰模式的异常.茶多酚具有抑制DNA甲基转移酶、改变组蛋白修饰和miRNA表达的生物学活性,对肿瘤的防护与治疗具有一定的价值.该文就茶多酚的表遗传机制的研究进展作一简要概述.

Abstract：

Tea polyphenols (TP) is one of components from green teas, beneficial to human health. They may help prevent different types of tumors, and are involved in epigenetic pathway. Epigenetics is defined as reversible heritable changes in gene expression that occur without alteration in DNA sequence, including DNA methylation, histone modification, chromatin remodeling, and RNA interference.Most of tumors in humans have shown the abnormal patterns of epigenetics. Tea polyphenols demonstrated some effects of epigenetic agents, inducing epigenetic changes through modifying methylation, histone modifications and expression of some miRNAs. It has potential to be used as an agent for tunor prevention.     

Antioxidant and antiapoptotic effects of green tea polyphenols against azathioprine-induced liver injury in rats

Green tea polyphenols (GTP) is considered to have protective effects against several diseases. The hepatotoxicity of azathioprine (AZA) has been reported and was found to be associated with oxidative damage. This study was conducted to evaluate the role of GTP to protect against AZA-induced liver injury in rats. AZA was administered i.p. in a single dose (50 mg kg⁻¹) to adult male rats. AZA-intoxicated rats were orally administered GTP (either 100 mg kg⁻¹ day⁻¹ or 300 mg kg⁻¹ day⁻¹, for 21 consecutive days, started 7 days prior AZA injection).AZA administration to rats resulted in significant elevation of serum transaminases (sALT and sAST), alkaline phosphatase (sALP), depletion of hepatic reduced glutathione (GSH), catalase (CAT) and glutathione peroxidase (GPx), accumulation of oxidized glutathione (GSSG), elevation of lipid peroxides (LPO) expressed as malondialdehyde (MDA), reduction of the hepatic total antioxidant activity (TAA), decrease serum total proteins and elevation of liver protein carbonyl content. Significant rises in liver tumor necrosis factor-alpha (TNF-α) and caspase-3 levels were noticed in AZA-intoxicated rats. Treatment of the AZA-intoxicated rats with GTP significantly prevented the elevations of sALT, sAST and sALP, inhibited depletion of hepatic GSH, GPx, CAT and GSSG and inhibited MDA accumulation. Furthermore, GTP had normalized serum total proteins and hepatic TAA, CAT, TNF-α and caspase-3 levels of AZA-intoxicated rats. In addition, GTP prevented the AZA-induced apoptosis and liver injury as indicated by the liver histopathological analysis. The linear regression analysis showed significant correlation in either AZA-GTP100 or AZA-GTP300 groups between TNF-α and each of serum ALT, AST, ALP and total proteins and liver TAA, GPX, CAT, GSH, GSSG, MDA and caspase-3 levels. However, liver TNF-α produced non-significant correlation with the serum total proteins in both AZA-GTP100 and AZA-GTP300 groups.In conclusion, our data indicate that GTP protects against AZA-induced liver injury in rats through antioxidant, anti-inflammatory and antiapoptotic mechanisms. However, further merit investigations are needed to verify these results and to assess the efficacy of GTP therapy to counteract the liver injury and oxidative stress status.