异位子宫内膜间质细胞中芳香化酶的表达及意义

目的探讨芳香化酶在异位子宫内膜间质细胞中的表达情况及其意义。方法体外培养正常和异位子宫内膜间质细胞,采用RT-PCR技术检测其中芳香化酶的表达,发光免疫法检测雌二醇(E2)的表达,流式细胞仪检测凋亡细胞。结果正常子宫内膜间质细胞不表达芳香化酶及E2,细胞凋亡率为7.52%±0.62%;异位子宫内膜间质细胞芳香化酶mRNA为0.89±0.04,E2为(77.24±10.45)pmol/L,细胞凋亡率为1.20%±0.9%,其细胞凋亡率明显低于正常子宫内膜间质细胞(P<0.05)。结论异位子宫内膜间质细胞可以利用芳香化酶合成内源性E2,从而促进细胞增殖。     

COX-2在子宫内膜异位症保守性手术后复发患者病变组织中的表达及意义

目的 探讨预防子宫内膜异位症(EMs)保守性手术后复发的方法.方法 对行保守性手术治疗的51例EMs(复发25例、未复发26例)患者(观察组)和10例卵巢单纯性囊肿患者(对照组),采用免疫组织化学方法检测病变组织中环氧合酶(COX)-2表达.结果 COX-2在观察组和对照组病变组织中的阳性表达率分别为74.50%和30.00%,P＜0.05;在观察组复发和未复发者病变组织中的阳性表达率分别为60.00%和88.46%,P＜0.05.结论 COX-2在EMs的发生、发展及复发中可能起重要作用,监测EMs患者术后病理标本中COX-2表达对术后治疗干预及预后有重要临床价值.     

COX-2基因多态性与子宫内膜异位症及子宫腺肌病关系的研究

目的探讨环氧合酶（COX）-2基因多态性与子宫内膜异位症（内异症）和子宫腺肌病的关系。方法用蛋白酶K消化—饱和酚氯仿法提取外周血白细胞DNA、PCR-限制性片段长度多态分析（PCR-RFLP）分别对70例内异症（EMs组）、50例子宫腺肌病（Ad组）和240例非内异症、腺肌病妇女（对照组）进行基因分型。结果EMs组、Ad组基因型频率COX-2-1195GG、AG和AA与对照组比较,具有显著性差异（P〈0.05）,前两组AA基因型频率及A等位基因频率均显著高于对照组,而EMs组和Ad组之间差异无显著性。携带2个A等位基因者患EMs的风险为对照组的2.67倍,患子宫腺肌病风险为对照组的3.02倍。结论COX-2-1195G〉A单核苷酸多态可能是决定EMs和子宫腺肌病个体遗传易感性的重要因素,两种疾病存在相似的遗传易感性。     

腹腔镜对子宫内膜异位症卵巢功能的探讨

３１５例子宫内膜异位症（ＥＭ）患者腹腔镜下卵巢所见显示：卵泡发育与周期时相关系，排卵征对判断卵巢功能有一定意义，本组卵泡发育异常９０例（６７．２％），排卵阳性４６．４％，排卵阴性５３．６％。高温期内膜病检，排卵符合率４２．５％，认为内膜病检作为判断排卵的辅助诊断，可靠性较低，本组测定泌乳素（ＰＲＬ）３９．６％高于正常，说明子宫内膜异位症与ＰＲＬ关系密切。同时对镜下观察卵巢功能的要领进行了介绍。     

结直肠子宫内膜异位症恶变的研究进展

子宫内膜异位症在育龄期妇女中是一种相对常见的病变,但肠道的子宫内膜异位组织恶变比较罕见。其病因未明,目前用以解释其起源的理论较多。尽管目前针对这种少见疾病无标准治疗方法,但是根治性手术结合术后辅助治疗的模式可作为一种治疗选择。     

输尿管子宫内膜异位症64例临床分析

15％～20％的育龄妇女患有子宫内膜异位症。病变多局限于卵巢、子宫骶韧带等部位,侵犯输尿管者较少见。输尿管子宫内膜异位症常缺乏典型症状,给诊断及治疗带来一定难度。现结合本院2000～2004年收治的4例,并复习近10年来相关文献报道的60例,对输尿管子宫内膜异位症的诊断及治疗方法进行分析。     

腹壁子宫内膜异位症8例临床分析

目的探讨腹壁子宫内膜异位症的临床特点及治疗方法。方法回顾性分析8例腹壁内异症患者的临床资料。结果8例腹壁子宫内膜异位症患者中,1例发生于子宫肌瘤剔除术后,7例发生于足月剖宫产术后,1例发生于孕中期剖宫取胎术后。8例均接受了手术治疗。术后随访1—3a,均无复发。结论腹壁子宫内膜异位症好发于剖宫产术后。手术是惟一有效的治疗方法。对较大、较深的病灶,适当扩大切除范围,达到切缘干净,是防止复发的关键。     

雌激素对子宫内膜细胞凋亡的影响及其机制探讨

目的 观察雌激素对子宫内膜细胞凋亡的影响,并探讨其机制.方法 将原代培养的子宫内膜细胞随机分为C组和E8、E7、E6组.C组不加雌激素,E8、E7、E6组分别加入浓度为10-8、10-7、10-6 mol/L的雌激素.采用流式细胞术检测细胞凋亡率,Real-time PCR法检测前列腺特异性酸性磷酸酶（PSAP）基因;构建PSAP基因干扰载体,并转染至子宫内膜细胞,观察转染前后细胞凋亡率和PSAP基因表达量.结果 C、E8、E7、E6组细胞凋亡率（gate1）分别为10.8％±0.1％、15.5％±0.2％、15.8％±0.1％、16.6％±0.3％,E8组和E7组比较,P＞0.05;其余两两比较,P均＜0.05.C、E8、E7、E6组细胞凋亡率（gate2）分别为4.2％±0.2％、4.5％±0.1％、5.4％±0.2％、5.7％±0.1％,两两比较,P均＜0.05.C、E8、E7、E6组PSAP基因表达量分别为0.46 ±0.05、0.33 ±0.03、0.26±0.03、0.40 ±0.02,两两比较,P均＜0.05.干扰前后细胞凋亡率分别为18.2％±1.3％、10.2％±0.7％,PSAP基因表达量分别为50.4 ±3.2、19.2±1.3,P均＜0.05.结论 雌激素作用后子宫内膜细胞凋亡增加,PSAP基因表达降低;PSAP基因被干扰后,细胞凋亡减少.雌激素可能通过抑制PSAP基因表达促进子宫内膜细胞凋亡.     

桂枝茯苓胶囊抑制子宫内膜异位症大鼠子宫内膜血管新生

目的探讨桂枝茯苓胶囊对子宫内膜异位症大鼠子宫内膜血管新生的作用机制。方法 80只雌性大鼠随机均分成空白对照组、模型组及桂枝茯苓胶囊低剂量组(0.5 g/kg)和高剂量组(1.5 g/kg),其中模型组、桂枝茯苓胶囊低剂量组和高剂量组均采用自体移植法建立大鼠子宫内膜异位症模型。桂枝茯苓胶囊低、高剂量组连续给药,模型组及空白对照组给予等体积的生理盐水,培养28 d后处死大鼠,采用免疫组织化学及荧光定量聚合酶链反应(PCR)检测大鼠子宫内膜组织中caveolin-1及血管内皮生长因子(VEGF)的表达,并对两者表达进行相关性分析。结果桂枝茯苓胶囊低、高剂量组caveolin-1的表达升高,而VEGF表达降低,相比于模型组差异有统计学意义(P0.05),其中桂枝茯苓胶囊高剂量组caveolin-1表达显著高于低剂量组(P0.05),而VEGF表达则显著低于低剂量组(P0.05),存在剂量依赖效应;VEGF表达与caveolin-1表达水平呈负相关(r_(低剂量组)=-0.65,P0.05;r_(高剂量组)=-0.61,P0.05)。结论桂枝茯苓胶囊能显著提高子宫内膜异位症大鼠caveolin-1蛋白的表达水平,其抑制血管生成的作用可能是通过调控caveolin-1蛋白与VEGF蛋白的相互作用来完成。     

直肠子宫内膜异位症误诊1例

病例:患者女,42岁,已婚已育。因间断性下腹痛伴黏液血便3年,加重2个月于2013年11月2日收治入院。入院时一般情况可,大便1次/d,排出不畅,带黏液血便。查体:心肺未见异常,腹平软,下腹部见纵形手术瘢痕,无压痛、反跳痛,未扪及腹部包块,移动性浊音(-)。肛检示距肛门口约4~5 cm处截石位12~2点可及一隆起灶,质硬、固定,表面欠光滑,结节状,局部压痛,指套染淡红色血迹和黏液。实     

Effect of DL-alpha-lipoic acid on glutathione metabolic enzymes in aged rats.

Ageing is characterized by a failure to maintain homeostasis under conditions of physiological stress, with an increasing susceptibility to disease and death. The accumulation of errors committed by faulty biochemical reactions over a vast period generates the cumulative effect observed during ageing. The most notable among the effects of ageing are the age-related disorders where free radicals are the major cause. When the level of free radicals increases because of diet, lifestyle, environment or other influences, it results in subsequent reduction of antioxidants. Reduced glutathione is one of the most fascinating molecules virtually present in all animal cells in often quite higher concentrations. An essential mechanism that accounts for most of the metabolic and cell regulatory properties of glutathione is the thiol disulfide exchange equilibria. We evaluated the age-associated alterations in glutathione dependent enzymes, glutathione and hydroxyl radicals in young and aged rats with respect to lipoate supplementation. In aged rats, activities of glutathione peroxidase, glutathione reductase, glutathione-S-transferase and glucose-6-phosphate dehydrogenase and the level of glutathione were low, whereas the level of hydroxyl radical was higher than in the young ones. Administration of DL-alpha-lipoic acid, a thiol antioxidant intraperitoneally to the aged rats, led to a time-dependent reduction in hydroxyl radicals and elevation in the activities/level of glutathione systems. Hence it can be suggested that lipoate, a dithiol prevents the oxidation of reduced glutathione and protects its related enzymes from peroxidative damage.     

非酒精性脂肪性肝病大鼠内生性乙醇和肝组织乙醇代谢相关酶的变化*

目的 观察高脂饮食和高果糖饮食对大鼠肝脏病理、内生性乙醇、乙醇代谢酶的影响。方法 将SD大鼠18只随机分为正常组（n=6）,予以普通饲料喂养,高果糖组（n=6）接受普通饲料和含20%果糖水喂养,高脂组（n=6）接受高脂饲料喂养。造模16 w后,取肝组织进行非酒精性脂肪性肝病活动性评分（NAS）;采用Biovison试剂盒检测门静脉血乙醇水平;采用实时荧光定量PCR法检测大鼠肝组织乙醇脱氢酶（ADH1）和乙醛脱氢酶（ALDH2）mRNA水平;采用Western blot法测定肝组织ADH1和ALDH2蛋白表达水平;使用乙醇脱氢酶活性试剂盒测定肝组织匀浆乙醇脱氢酶活性。结果 在16 w末,高果糖组大鼠肝组织表现为脂肪变性,高脂组大鼠肝组织主要表现为NASH;高脂组大鼠NAS评分为5.40±0.32,显著高于对照组【（1.10±0.25）,P<0.05】和高果糖组【（2.94±0.40）,P<0.05】 ;高脂组大鼠血清内生性乙醇水平【（1.30±0.15）nmol/μL】显著高于正常组【（1.00±0.10）nmol/μL,P<0.05）】和高果糖组【（1.04±0.23）nmol/μL,P<0.05）】;高脂组大鼠ADH1 mRNA水平显著高于正常组（（1.30倍,P<0.05）和高果糖组（1.36倍,P<0.05）;高脂组大鼠ALDH2mRNA水平显著高于正常组（1.55倍,P<0.05）和高果糖组（1.44倍,P<0.05）;高脂组大鼠ADH1蛋白表达显著高于正常组（2.56倍,P<0.05）和高果糖组（2.52倍,P<0.05）;高脂组大鼠ALDH2蛋白表达显著高于正常组（1.41倍,P<0.05）和高果糖组（1.57倍,P<0.05）;高脂组大鼠肝脏乙醇脱氢酶活性为（175±28）μ/L,显著高于正常组【（72±13）μ/L,P<0.05）】和高果糖组【( 78±9)μ/L,P<0.05）】。结论 高脂饮食造模大鼠内生性乙醇浓度显著升高,乙醇脱氢酶和乙醛脱氢酶蛋白水平升高,乙醇脱氢酶活性显著升高。     

雌激素对去卵巢大鼠血管钙化的影响

目的:探讨雌激素对去卵巢大鼠血管钙化的影响.方法:将40只雌性SD大鼠随机分为5组,每组8只.空白对照组正常喂养.去卵巢钙化组、β2雌二醇(E2)溶媒对照组和E2干预组均切除双侧卵巢,假手术钙化组切除卵巢周围等体积的脂肪组织,术后给予维生素D3 30万U·kg-1·.d-1注射3d建立血管钙化模型.E2溶媒对照组和E2...     

雌激素对大鼠实验性自身免疫性甲状腺炎的影响

目的　研究雌激素在诱发实验性自身免疫性甲状腺炎 (EAT)形成中的影响。方法　 10周龄Wistar大鼠进行双侧卵巢切除术后采用同种属SD大鼠甲状腺球蛋白 (Tg)免疫诱发EAT。病理切片HE染色观察甲状腺炎症反应。采用放免方法测定血清中E2 、PRL水平。间接酶联免疫吸附实验 (ELISA )测定血清Tg抗体 (TgAb)水平。逆转录 聚合酶链反应 (RT PCR)检测甲状腺组织中γ 干扰素 (IFN γ)、白细胞介素 10 (IL 10 )mRNA的表达水平。结果　大鼠切除双侧卵巢后 ,其血清中雌二醇 ( 17.60± 1.0 2 )pmol/L和PRL( 2 .45± 0 .15 ) μg/L水平明显低于未切除卵巢组〔分别为 ( 5 8.5 6± 6.99) pmol/L和 ( 3 .2 2± 0 .17) μg/L〕(均P <0 .0 1) ,实验性自身免疫性甲状腺炎的发病率和甲状腺组织中炎细胞浸润程度也均较未切除卵巢直接诱发EAT组明显减轻 ,甲状腺组织中IFN γmRNA的表达水平 ( 0 .87± 0 .0 3 )较未切除卵巢直接诱发EAT组 ( 0 .99± 0 .0 0 )明显下降 (P <0 .0 5 ) ,而IL 10mRNA的表达水平 ( 0 .98± 0 .0 1)则高于未切除卵巢直接诱发EAT组 ( 0 .83± 0 .0 5 )。诱发为EAT的两组大鼠血清TGAb平均水平 ( 1.3 9± 0 .0 3 )明显高于非诱发EAT对照组的平均水平 ( 0 .18± 0 .0 0 )(P <0 .0 1)。结论　雌激素水平低下可     

Effect of high intratesticular estrogen on the seminiferous epithelium in adult male rats

The presence of estrogen receptor beta and aromatase in the germ cell has highlighted the physiological role of the traditionally female hormone, estrogen, in spermatogenesis. Estrogen receptor alpha knockouts and aromatase knockouts have further accentuated the role of estrogen in germ cell maturation. To delineate the direct action of estrogen in the seminiferous epithelium, we studied the effects of high intratesticular estradiol. The study was based on the fact that administration of exogenous estradiol suppresses the hypothalamus pituitary gonadal axis (HPG) with a dose-dependant concomitant increase in intratesticular estrogen levels. Three doses of 17-beta estradiol, namely 20, 100 and 200 microg/kg/day were administered subcutaneously to different batches of adult male rats for 10 days. The effect of the three doses on serum hormonal profile, intratesticular testosterone (T) and estradiol (E) levels were studied. Twenty micrograms per kilograms per day of 17-beta estradiol affected the hypothalamus-pituitary axis, reducing serum gonadotropins and intratesticular testosterone; however, 100 microg/kg/day of 17-beta estradiol decreased serum FSH and intratesticular testosterone, increased intratesticular estradiol, but had no effect on serum LH. Interestingly, 200 microg/kg/day of 17-beta estradiol decreased serum and intratesticular T without any effect on serum gonadotropins. This could be attributed to the positive feedback effect of estrogens on gonadotropins. In the testis, morphologically two visible effects were seen, namely 'spermiation failure' in all three doses attributed to the suppression of T and FSH and a 'maintenance effect' in the 100 microg/kg/day attributed to E and/or 10% of available intratesticular T. The direct effect of an increase in intratesticular estradiol levels was observed in terms of a decrease in apoptosis in germ cell. The study, therefore, suggests that 100 microg/kg/day of 17-beta estradiol could be used to study the effects of high intratesticular estradiol with a concomitant decrease in intratesticular T and serum FSH levels on spermatogenesis.     

Effect of ovariectomy on renal estrogen receptor-alpha and estrogen receptor-beta in young salt-sensitive and -resistant rats

This study evaluated the effect of ovariectomy on renal estrogen receptor (ER)-alpha and ERbeta expression in young female Dahl salt-sensitive and salt-resistant rats. Our hypothesis was that estrogen depletion results in an imbalance in ERalpha and ERbeta expression in salt-sensitive rats. Rats were subjected to sham surgery (intact), ovariectomy, and ovariectomy with estrogen replacement. Kidneys were harvested 8 weeks later. Western blot was used to measure ERalpha and ERbeta expression in the cortex and medulla. In intact rats, ERalpha was 2.7- and 4.3-fold higher in salt-sensitive compared with salt-resistant rats in the renal cortex and medulla, respectively. In salt-sensitive rats, ovariectomy caused 42% and 52% decreases in ERalpha and 107% and 314% increases in ERbeta in renal cortex and medulla, respectively. In salt-resistant rats, ovariectomy caused 33% and 150% increases in ERalpha and 107% and 100% increases in ERbeta in renal cortex and medulla, respectively. Estrogen replacement did not alter ERalpha but restored ERbeta expression levels similar to levels in intact rats in both salt-sensitive and salt-resistant rats. Thus, estrogen loss had opposite effects on ERalpha in salt-sensitive (downregulation) and salt-resistant rats (upregulation). We propose that the decrease in ERalpha expression in salt-sensitive rats after estrogen loss alters the balance of renal ERs and may play a role in accelerating the development of hypertension and renal damage.