大剂量雌二醇对大鼠胸腺的影响

本研究用大剂量苯甲酸雌二醇,诱导性成熟前SD大鼠的胸腺迅速退化,可见皮质明显变薄,皮、髓质比例降低,皮质内淋巴细胞大量减少。电镜下见胸腺的上皮性网状细胞(ERC)为一异质性细胞群,它们对雌二醇的反应性也各不相同。其典型的改变为:1.一部分明ERC呈明显的退行性变;2.另一部分明ERC内则充满低电子密度的囊泡;3.暗ERC明显增多,该细胞胞体及其突起的周围,都有许多胶原原纤维。血管周围间隙内也呈类似改变。淋巴细胞的超微结构虽未见异常,但胸腺内酸性非特异性酯酶(ANAE)阳性的T细胞数,明显低于对照组。胸腺皮质内有大量浆细胞聚集,其粗面内质网多高度扩张。本文在上述形态学观察基础上,就雌二醇诱导胸腺退化的机制进行了讨论。     

烫伤大鼠血淋巴细胞bcl-2、bcl-x和bax的表达及作用

目的 :研究大鼠烫伤后外周血淋巴细胞的凋亡及其bcl 2家族基因的表达 ,以探讨烫伤后bcl 2家族基因的表达对细胞凋亡的调控。方法 :复制 30 %体表面积Ⅲ度烫伤大鼠模型 ;分离外周血淋巴细胞 ,TUNEL荧光标记 ,流式细胞仪分析细胞凋亡 ;提取总RNA ,采用RT PCR分析bcl 2家族调控基因的表达。结果 :外周血淋巴细胞凋亡在健康大鼠比例较低 ( 3.99± 1 .72 % ) ,但伤后各组 ( 3、6、1 2、2 4、4 8h依次分别为 8.5 8± 1 .5 3%、8.38± 1 .81 %、2 0 .77± 3.94 %、2 3.90± 3.92 %和 1 1 .2 1± 1 .35 % )均明显增加 (P <0 .0 1 ) ,以伤后…     

环磷酰胺诱发大鼠胸腺细胞凋亡的研究

目的：研究环磷酰胺的免疫抑制作用机制。方法：以大鼠胸腺为对象,采用细胞凋亡的原位特异性染色及ＤＮＡ凝胶电泳的方法,观察没剂量、不财时间环磷酰胺处理后胸腺细胞的凋亡现象。结果：剂量为２０和７０ｍｋ／ｋｇ的环磷酰胺可引起广泛的胸腺细胞凋亡。该作用最早发生在环磷酰胺处理后的８Ｈ,１２～２４最明显,４８Ｈ消失。结论：环磷酰胺的免疫作用可能是通过诱导免疫细胞凋亡而产生的。     

大黄对大鼠脑缺血一再灌注损伤bcl-2、bax表达的影响

目的探讨大黄对大鼠脑缺血-再灌注损伤过程中的抗凋亡作用及机制。方法SD大鼠64只分假手术组、模型组、大黄组和尼莫地平组,每组16只。线栓法制作大鼠脑缺血再灌注模型,以HE染色和免疫组化的方法观察大黄0.45g/(kg·d)、尼莫地平1mg/(kg·d)对大鼠大脑海马回CA1区细胞形态以及bcl-2、bax蛋白表达的细胞数目。结果大黄组显示海马回细胞病理改变较模型组差异显著,bcl-2表达水平增高(P<0.05),bax表达水平降低(P<0.05),bcl-2/bax的表达比例增加(P<0.05),大黄组和尼莫地平组差异无显著意义(P>0.05)。结论大黄有明显减少脑梗死边缘区域凋亡水平的作用,其机制与bcl-2表达增高,bax表达降低,降低bcl-2/bax值有关。     

甲状腺激素缺乏对大鼠胸腺细胞凋亡的影响

目的:探讨甲状腺激素缺乏对大鼠胸腺细胞凋亡及其相关蛋白Bcl-2和Bax表达的影响.方法:采用放射免疫技术测定甲巯咪唑组仔鼠血清中三碘甲状腺原氨酸(T3)、四碘甲状腺原氨酸(T4)、促甲状腺激素(TSH)水平;应用光镜、透射电镜技术和共聚焦激光扫描显微镜观察胸腺组织细胞形态学改变;免疫组织化学法检测胸腺组织中Bcl-2和Bax蛋白的表达.结果:甲巯咪唑组仔鼠体小,行动迟缓,胸腺绝对质量明显低于对照组,差异有统计学意义.对照组大鼠血清中T3、 T4值均高于甲巯咪唑组,TSH值低于甲巯咪唑组.甲巯咪唑组胸腺组织中出现大量的凋亡细胞和凋亡小体.Bcl-2蛋白表达的平均光密度值低于对照组;胸腺组织中Bax蛋白表达的平均光密度值高于对照组.结论:甲状腺激素缺乏可抑制胸腺组织中Bcl-2蛋白的表达和促进Bax蛋白的表达,诱导大鼠胸腺细胞凋亡,促进胸腺退化.     

丙酸睾酮对大鼠胸腺细胞凋亡及胸腺中Bcl-2、Bax表达的影响

目的探讨丙酸睾酮在大鼠胸腺退化过程中的作用及其对大鼠胸腺中Bcl-2和Bax表达的影响。方法雄性大鼠去势后给予丙酸睾酮皮下注射,分别于注射后第1、4、7天取材,用半薄切片甲苯胺蓝染色检测胸腺细胞凋亡情况,免疫组织化学法检测胸腺组织中Bcl-2和Bax的表达情况,采用t检验进行统计学处理。结果丙酸睾酮处理组大鼠胸腺组织中可发现较多的凋亡细胞和凋亡小体;去势组大鼠胸腺组织中Bcl-2表达量明显高于假手术组（P〈0.001）,丙酸睾酮处理后Bcl-2表达量明显减少（P〈0.001）;而Bax的表达正好相反,去势组大鼠胸腺组织中Bax表达量明显低于假手术组（P〈0.001）,给予丙酸睾酮后Bax表达量明显增加（P〈0.001）;结论丙酸睾酮可诱导大鼠胸腺细胞凋亡,并抑制大鼠胸腺组织中Bcl-2的表达,促进Bax的表达。     

雌性去胸腺大鼠及老年大鼠下丘脑LHRH,血浆雌二醇和肝细胞浆雌二醇受体的变化

雌性成年去胸腺大鼠(8月龄;于2月龄时切除胸腺,术后6月处死进行实验)和老年大鼠(24月龄)下丘脑黄体生成素释放因子(LHRN)和血浆雌二醇(E_2)水平降低,肝细胞浆雌二醇受体(E_2-R)与E_2结合的解离常数Kd值是减小趋势,受体浓度有所提高。以上变化均以老年大鼠更明显。推测肝胞浆雌二醇受体的变化可能是由于血浆E_2水平降低引起受体向上调节所致。     

雌激素对大鼠胸腺细胞凋亡及Bcl-2、Bax表达的影响

目的:探讨苯甲酸雌二醇对大鼠胸腺Bcl-2和Bax表达及细胞凋亡的影响及其机制.方法:雌性大鼠行卵巢切除术,给予苯甲酸雌二醇后,观察胸腺指数的变化,Hochest33342荧光染色及透射电镜标本观察胸腺细胞凋亡情况,免疫组织化学检测胸腺组织中Bcl-2和Bax的表达情况,原位杂交技术检测Bcl-2、Bax m RNA的表达情况.结果:双侧卵巢切除组大鼠胸腺指数较假手术组增加,双侧卵巢切除+雌激素组大鼠胸腺指数较双侧卵巢切除组减小;假手术组和双侧卵巢切除组大鼠胸腺组织中以正常胸腺细胞为主,偶见凋亡细胞或凋亡小体,双侧卵巢切除+雌激素组可见较多凋亡细胞和凋亡小体;双侧卵巢切除+雌激素组大鼠胸腺组织中Bcl-2表达较双侧卵巢切除组和假手术组增高明显降低,而Bax表达呈现相反趋势;Bcl-2 mRNA、Bax mRNA的表达与Bcl-2、Bax的表达呈一致性.结论:雌激素可以降低大鼠胸腺指数,抑制胸腺组织中Bcl-2的表达,促进Bax的表达,从而诱导大鼠胸腺细胞凋亡,促进雌性大鼠胸腺退化.     

两种小鼠胸腺基质细胞对胸腺细胞凋亡的不同作用

采用两种体外建系的小鼠胸腺基质细胞（ＴＳＣ）系，即上皮样ＴＳＣ（ＭＴＥＣ１）和树突状ＴＳＣ（ＭＴＳＣ４），观察其对胸腺细胞凋亡的影响。小鼠胸腺细胞在体外培养过程中，可自发地出现细胞凋亡的特征，表现为ＤＮＡ呈梯度断裂片段，细胞经ＦＡＣＳ分析出现亚二倍体ＤＮＡ波峰，以及Ｆｅｕｌｇｅｎ′ｓ染色镜检所见的ＤＮＡ凝聚和断裂。胸腺细胞在与ＴＳＣ共育后，在ＭＴＥＣ１组可见其凋亡过程受到抑制和存活率的增加；在ＭＴＳＣ４组，仅在共育１２至１８小时时，见到胸腺细胞凋亡加强，而其存活率不受影响。结果提示在胸腺细胞发育过程中，其阴性选择作用的主要机制之一的ＰＣＤ过程受不同来源的胸腺基质细胞的调节。     

高温对神经细胞凋亡及bcl-2和bax表达的影响

通过神经细胞原代培养并给予高温刺激 ,应用 TUNEL检测、免疫细胞化学和图像分析技术 ,研究了高温对神经细胞凋亡及凋亡相关基因 bcl- 2和 bax表达状况的影响。结果显示 ,TU NEL方法可在原位检测单个凋亡细胞 ,且较敏感 ,高温处理使细胞凋亡数明显增加 ,bcl- 2和 bax出现异常表达。表明高温可诱发原代培养神经细胞凋亡 ,bcl- 2和 bax发挥作用。     

The Effect of Cyproterone Acetate and Estradiol Benzoate on the Adrenal Gland of Juvenile and Adult Rats: A Morphometrical Study

Little is known about the effect of antiandrogens and estrogens on the adrenal cortex. To investigate their influence the antiandrogen Cyproterone acetate (CP) and the estrogen estradiol benzoate (EB) were applied separately to matched groups of animals. While EB affects the hypothalamic-pituitary axis via a negative feedback mechanism, CP has a competitive influence on peripheral androgen receptors and also affects the central regulatory mechanism through its gestagenic component.48 male rats were divided in 6 groups, two for CP, two for EB, two control, each pair consisting of half young, half adult animals. Animals were killed on the 36th day of the assay. The histologic slides of adrenal tissue were evaluated using microphotographs enlarged by copyprint to 800fold magnification.The effects of the two drugs are recorded separately for the three zones of the Adrenal cortex, Z. glomerulosa (ZG), Z. fasciculata (ZF) and Z. reticularis (ZR): EB provokes atrophy of ZG in young rats, whereas no effects of CP on this zone are registered morphometrically in young nor in adult animals. ZF shows marked regressive transformation and CP, stronger in adult than in young animals. EB causes regressive transformation only in young rats. The effects of CP on ZR in different in young and adult rats, the young ones showing marked atrophy, the adult group demonstrating an increase of cell volume, — EB-treated rats, both young and adult, show a volume increase of reticularis cells.ZG-atrophy under EB is not adequately explained by the morphological methods used in our assay. The regressive transformation of ZF in young and adult rats seems to be due to an additional corticotropic action of CP, whereas the progressive transformation under EB is probably due to the paradoxical effect of estrogens with a positive feedback mechanism. The diversity of ZR reactions to CP is explained by different steroid metabolisms in the groups. The volume increase of reticularis cells under EB may be due to an increased storage of steroid precursors.     

咖啡酸锗对小鼠U14瘤的抑制作用及其诱导肿瘤细胞凋亡的机制研究

目的：研究咖啡酸锗对荷瘤U14小鼠的体内抑瘤作用及体外抗肿瘤活性，探讨其抗肿瘤作用机制。方法：观察咖啡酸锗对小鼠U14宫颈癌的抑制率；用MG-P染色和透射电镜的方法观察肿瘤细胞的凋亡情况；流式细胞术(FCM)观察瘤组织的细胞凋亡率并分析细胞周期；免疫组化方法观察肿瘤组织中Bax和Bcl-2蛋白表达情况；MTT法评价咖啡酸锗体外抑制U14肿瘤细胞活性。结果：咖啡酸锗低、中、高剂量组对宫颈癌U14的抑瘤率分别为38.50％、47.17％和64.04％（P<0.01）。MG-P染色及电镜观察可见，咖啡酸锗治疗组出现较多的凋亡细胞（P<0.05），可见典型的细胞凋亡的形态学特征。流式细胞术检测表明咖啡酸锗能诱导U14肿瘤细胞凋亡，在G₀-G₁前出现1个明显的凋亡峰，细胞被阻滞在S期。咖啡酸锗处理后肿瘤组织中Bcl-2蛋白表达下调，Bax蛋白表达上调。咖啡酸锗对体外培养的U14细胞增殖均有一定程度的抑制作用，48 h的IC₅₀值为48.57 mg/L。结论：咖啡酸锗在体内、外均能有效抑制小鼠U14瘤细胞的增殖，并诱导肿瘤细胞凋亡。咖啡酸锗上调U14细胞中Bax蛋白的表达，下调Bcl-2蛋白的表达，进而促进肿瘤细胞凋亡，这可能是其发挥抗肿瘤作用的机制之一。     

氨茶碱对哮喘豚鼠嗜酸细胞凋亡及bcl—2 mRNA表达的影响

目的 观察氨茶碱对体外不同密度嗜酸细胞（Eos）凋亡及bcl-2 mRNA表达的影响,探讨其促进哮喘Eos凋亡的机制。方法 卵蛋白激发哮喘豚鼠动物模型48h后行支气管肺泡灌洗,分离不同密度Eos。氨茶碱（AM）（10^-6-10^-3mol/L)干预24h,原位杂交检测Eos的bcl-2 mRNA表达,TUNL法检测细胞凋亡。结果 AM干预24h,可见Eos凋亡增加,以低密度Eos(HEos)为明显,bcl-2 mRNA表达,呈剂量依赖性。bcl-2 mRNA的表达与Eos凋亡呈负相关。结论 AM可抑制bcl-2 mRNA表达,促进Eos凋亡。bcl-2参与了AM对Eos凋亡的调节。     

注射用雌二醇聚乳酸羟基乙酸缓释微球生物相容性研究

目的：以整体动物为研究对象，考察注射用雌二醇聚乳酸羟基乙酸缓释微球动物体内的生物降解和生物相容性。方法：肌注给药，显微镜观察组织切片，研究空白PLGA微球及载雌二醇PLGA微球的生物降解和相容性。结果：28d内，微球从规则球形降解为不规则微小颗粒，组织学观察空白微球和载雌二醇微球均未见病理改变。结论：注射用雌二醇聚乳酸羟基乙酸缓释微球具有良好的生物降解和相容性。     

Two relatively distinct patterns of ameloblastoma: an anti-apoptotic proliferating site in the outer layer (periphery) and a pro-apoptotic differentiating site in the inner layer (centre)

AIMS: This study was performed to determine the apoptotic behaviour of ameloblastomas by analysing the role of bcl-2 family proteins in ameloblastomas and the location of terminally apoptotic cells in the ameloblastoma epithelial tissues. METHODS AND RESULTS: For immunohistochemistry, tissue sections of 32 patients were treated with an antigen-retrieval METHOD: Primary antibodies against the apoptosis-related proteins, bcl-2, bcl-X, bax, and bak were applied. Besides immunohistochemistry, Western blotting and TUNEL were also performed. Most of the outer layer cells were predominantly stained by the bcl-2 antibody, while most of the inner layer cells were stained by antibodies against the apoptosis-modulating proteins, bax and bak. Among the bcl-2 family, bcl-2 was the most ubiquitously expressed protein in ameloblastomas, while bcl-X was expressed in the greatest concentrations. The major bcl-X protein was bcl-XL. Some of the inner layer cells entered the terminal apoptotic stage, which were revealed by TUNEL. The acanthomatous areas over-expressed the apoptosis-modulating proteins, especially bak. CONCLUSIONS: Ameloblastoma has much more apoptosis-inhibiting protein than the apoptosis-modulating protein. Ameloblastoma has two relatively distinct patterns, an anti-apoptotic proliferating site in the outer layer (periphery) and a pro-apoptotic differentiating site in the inner layer (centre). The acanthomatous area, which was stained strongly by bak antibody and contained numerous terminally apoptotic cells, was considered as the differentiated area.     

Role of Capsaicin-Sensitive Neurons in the Regulation of Structural Organization of the Thymus

Anatomical organization of the thymus was studied in adult Wistar rats after injection of a neurotoxic dose of capsaicin. The reaction of the lymphoid parenchyma attested to depletion of structural reserves and triggering of autoimmunization mechanisms and was associated with accumulation thymocytes with morphological signs of apoptosis, Hassal's bodies, macrophages, plasmacytes, and eosinophils in the subcapsular zone. Through neurokinin and vanilloid receptors on the sensory terminals and lymphocytes, capsaicin modulated the level of neuropeptides, which seemed to be involved in the regulation of autoimmune mechanisms. __________ Translated from Byulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 140, No. 8, pp. 222–226, August, 2005     

新生大鼠缺氧缺血性脑损伤对脾bcl-2/bax/fas/fasL mRNA的影响

目的 通过检测脾淋巴细胞凋亡基因bcl-2/bax/fas/fasL mRNA表达水平,探讨缺氧缺血性肭损伤(hypoxicischemic brain damage,HIBD)脾细胞凋亡基因的变化与缺氧时间的关系,以此提供HIBD对于免疫功能影响的理论基础.方法 建立新生大鼠HIBD模型测定脾bcl-2/bax/fas/fasL mRNA 的相对表达量.结果 bcl-2处理组相对表达量低于对照组(P＜0.01).bax处理组相对表达量高于对照组(P＜0.01).bcl-2/bax处理组比值低于相应对照组(P＜0.05).fas处理纽相对表达量高于对照组(P＜0.01).fasL 1 h和6 h处理组相对表达量高于对照组,12 h之后则对照组远高于处理组.fas/fasL对照组较分散,除6 h组外其余组均小于1,处理组较集中,除24 h外均大于1.结论 HIBD可促进脾细胞促凋亡基因的表达,减少抑凋亡基因表达;HIBD发生6～12 h是促凋亡基因和抑凋亡基因高峰表达期;HIBD加强了fas/fasL的作用.     

人肺癌细胞凋亡与p53、bcl-2、Bax的表达

目的：探讨人肺癌组织细胞自发凋亡的发生,ｐ５３基因及凋亡相关基因ｂｃｌ－２、Ｂａｘ在肺癌组织中的表达及与肺癌细胞凋亡和生物学行为的关系。方法：用甲基绿－派诺宁染色检测５０例肺癌组织切片中凋亡细胞,ＬＳＡＢ免疫组化法检测ｐ５３和Ｂａｘ的蛋白表达,原位杂交方法检测ｂｃｌ－２ ｍＲＮＡ的表达。结果：１００％小细胞肺癌凋亡发生数１０个／ＨＰＦ,２１％的肺鳞癌和１５％的肺腺癌凋亡发生数〉１０个／ＨＰＦ。ｐ５