雌激素对大鼠去卵巢后白细胞介素-6介导的骨吸收的影响

目的观察雌激素对去卵巢大鼠骨髓细胞白细胞介素6(IL6)、IL6受体、gp130基因表达以及骨髓源性破骨细胞形成的影响。方法健康3月龄雌性SD大鼠72只,随机平均分为假手术对照组、去卵巢组和雌激素组(苯甲酸雌二醇02mg/kg,皮下注射,每周1次)。分别于术后2、4、6、12周每组各取6只大鼠骨髓细胞作细胞培养和提取RNA。培养第6天计数破骨细胞数,第12周取左侧胫骨作骨形态计量学检测。结果骨形态学显示去卵巢后出现骨吸收亢进,雌激素对其有抑制作用。去卵巢后2周,去卵巢组破骨细胞形成数即多于对照组(1450±169对901±141,P<005),骨髓细胞IL6和IL6受体mRNA表达均显著升高(P<005,P<001),第4～6周,上述改变达高峰,至第12周仍呈有意义增高;从2～12周,上述各指标雌激素组均明显低于去卵巢组(P<005,P<001)。各组未见gp130基因表达水平有明显变化。结论雌激素可以抑制大鼠去卵巢后骨髓源性破骨细胞的生成,这一效应可能与其抑制骨髓细胞在去卵巢后过度表达IL6、IL6受体基因有关。     

杜仲叶醇防治糖尿病合并去势大鼠骨质疏松症的实验研究

目的 探讨杜仲叶醇在治疗糖尿病(DM)合并去势大鼠骨质疏松症中的作用。方法 3月龄雌性Wistar大鼠50只，随机分成五组，每组10只(正常对照组、DM模型组、DM模型加中药组、DM合并去势组及DM合并去势加中药组)。用腹腔注射链脲佐菌素法制备DM大鼠模型，在此基础上用切除大鼠双侧卵巢的方法建立DM合并去势大鼠骨质疏松模型，以杜仲叶醇提取物为实验药物，通过测定各组大鼠的股骨线密度、面密度及雌激素含量，研究杜仲对DM合并去势大鼠骨质疏松症的作用。结果 杜仲叶醇提取物能提高DM合并去势大鼠的服骨线密度、面密度及其血清雌二醇含量。结论 杜仲叶醇提取物可阻止DM合并去势大鼠骨丢失，并具有类雌激素样作用。     

去卵巢大鼠骨髓源性破骨样细胞增殖、分化的改变及雌激素的影响

目的　通过体外骨髓细胞培养诱导破骨样细胞 (osteoclast likecells ,OLC)的形成 ,观察去卵巢对成年大鼠OLC形成及活性的影响以及给予雌激素后的改变。　方法　 3月龄SD大鼠分为对照组、去卵巢组及雌激素替代组。术后 12周处死大鼠 ,取股骨分离骨髓细胞 ,在条件培养液中诱导其向破骨细胞分化。活体观察OLC形成情况并于培养的第 6天行细胞染色 ,以抗酒石酸酸性磷酸酶(TRAP)染色 (+)、细胞核≥ 3个的细胞为OLC ,计数各组OLC及骨陷窝。　结果　 3组中去卵巢组OLC出现早且数量〔(2 7 75± 0 92 )个 /玻片〕明显高于其它两组〔(17 93± 0 6 9)个 /玻片和 (12 81±0 6 1)个 /玻片 ,P <0 0 1〕。雌激素处理能明显抑制OLC的形成 ,但雌激素替代组的OLC仍多于对照组 (P <0 0 5 )。骨陷窝形成的变化与OLC数量改变一致。　结论　本实验结果显示大鼠去卵巢后 ,骨髓干细胞分化形成OLC数量明显增多 ,且活性增强。补充雌激素能够有效抑制OLC形成增加及其活性增强。故雌激素抑制骨吸收的机制至少部分是作用于骨髓干细胞向破骨细胞的分化。     

年龄相关的骨髓细胞分化对成骨和破骨影响的实验研究

目的　从骨髓细胞分化角度研究年龄相关的成骨和破骨细胞分化的机理 ,探讨老年性骨质疏松症的发生机理。方法　通过骨髓细胞培养 ,应用组织形态学、流式细胞仪分析和分子生物学技术 ,采用碱性磷酸酶 (AL P)染色和骨钙素检测等手段观察青年大鼠和老年大鼠骨髓细胞分化成成骨和破骨细胞的状况。结果　青年大鼠骨髓基质细胞 (MSCs)形成成骨细胞数比老年大鼠多 (P<0 .0 1 ) ;老年大鼠骨髓细胞形成破骨细胞数比青年大鼠多 (P<0 .0 1 )。结论　大鼠骨髓细胞分化成成骨细胞的能力与年龄呈负相关 ,分化成破骨细胞的能力与年龄呈正相关。     

更年甘露饮加小剂量雌激素对去势大鼠股骨的影响

目的通过观察更年甘露饮加小剂量雌激素对去势大鼠股骨的影响，探索一种防治女性绝经期骨质疏松的新方法。方法雌性大鼠切除双侧卵巢预防用药3个月，检测各组大鼠血清激素水平、股骨骨密度（BMD）、光镜观察股骨结构，透射电镜观察子宫内膜腺上皮细胞超微结构。结果小剂量雌激素无改善作用，更年甘露饮加小剂量雌激素、常规剂量雌激素及更年甘露饮均能改善血清激素水平、股骨BMD及结构，其中更年甘露饮效果最弱，常规剂量雌激素对子宫内膜腺上皮细胞有明显刺激作用。结论更年甘露饮加小剂量雌激素改善去势大鼠血清激素水平、股骨BMD及结构的作用与单纯使用雌激素相似，对子宫内膜腺上皮细胞无明显刺激作用，可作为一种防治绝经期后女性骨质疏松的新方法。     

雌激素对实验性骨质疏松骨组织Ⅰ型胶原和基质金属蛋白酶-9表达的影响

目的探讨绝经后骨质疏松症发生的分子机制以及雌激素作用的分子环节。方法通过斑点杂交和原位杂交技术,研究卵巢摘除大鼠骨组织Ⅰ型胶原和基质金属蛋白酶－９（ＭＭＰ－９）ｍＲＮＡ表达及分布。结果骨质疏松时骨组织Ⅰ型胶原较正常组增加３倍,而ＭＭＰ－９表达均较正常组高４倍,雌激素替代治疗后,两基因表达下降。Ⅰ型胶原ｍＲＮＡ定位于成骨细胞,而ＭＭＰ－９则主要在破骨细胞、衬细胞和一些骨髓单核细胞（包括破骨细胞前体细胞）中表达。结论雌激素可通过影响骨形成和骨吸收相关基因的表达水平,降低骨转换率,发挥预防和治疗骨质疏松的作用     

Fas／FasL、FAP-1在肝母细胞瘤中的表达研究及其临床意义

目的 探讨肝母细胞瘤组织Fas、FasL及FAP-1和组织中淋巴细胞的Fas、FasL的表达状况及临床意义。方法 应用Fas、FasL多克隆抗体及FAP-1单克隆抗体对15例小儿肝母细胞瘤组织标本进行免疫组化染色，以检测其组织Fas、FasL及FAP-1和淋巴细胞的Fas、FasL的蛋白表达，并以相应的正常肝组织作对照。结果 肝母细胞瘤组织中Fas表达（78％）高于正常肝组织（5％），阳性信号主要位于细胞膜和细胞浆，呈胞浆型表达。正常肝组织中FasL表达阴性，而肝母细胞瘤中FasL表达73％，两者表达率差异明显；在15例肝母细胞瘤中FAP-1阳性表达13例。同时发现瘤周淋巴细胞Fas、FasL的阳性表达率分别为80％、68％，而在正常肝组织中的表达均为阴性。结论 正常肝组织同时表达Fas／FasL，在维持其自身细胞的增殖与凋亡的平衡中起重要作用；肝母细胞瘤组织Fas、FasL表达上调以及FAP-1阳性表达可诱导表达Fas的淋巴细胞凋亡以实现免疫逃逸。     

晚期氧化蛋白终产物对破骨细胞分化的影响

目的探讨晚期氧化蛋白终产物(AOPPs)对破骨细胞分化的影响。方法体外分离培养大鼠骨髓单核细胞,分为空白对照组、阴性对照组(RSA)、AOPPs组、阳性对照组(RANKL)、还原型烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶抑制剂组(AOPPs+夹竹桃麻素),干预6 d后,通过抗酒石酸酸性磷酸酶(TRAP)染色观察TRAP阳性多核细胞,鬼笔环肽荧光染色观察F肌动蛋白(F-actin)环,甲苯胺蓝染色观察骨磨片的骨吸收陷窝。此外,AOPPs刺激2 h后,通过DCFH-DA荧光探针法检测细胞内活性氧(ROS)生成。结果 AOPPs及阳性对照组RANKL均可诱导TRAP阳性多核细胞、F-actin环及骨吸收陷窝形成,并且AOPPs刺激后细胞ROS生成明显增多。AOPPs所致以上效应均能被NADPH氧化酶抑制剂夹竹桃麻素阻断。结论 AOPPs可诱导大鼠骨髓单核细胞向破骨细胞分化。     

补骨制剂Ⅱ对摘除卵巢大鼠骨质疏松的防治作用

目的研究补骨制剂Ⅱ经灌胃给药后对摘除卵巢大鼠骨质疏松模型的影响。方法雌性6月龄SD大鼠分为假去势组,模型组,阳性对照组,补骨制剂Ⅱ高、中、低剂量组(n=12),除假去势组进行假手术外,其余均手术彻底摘除卵巢法,术后进行模型筛选,9 d后假去势组、去势组均给予生理盐水,阳性对照组灌胃给予己烯雌酚0.02 mg/kg、鱼肝油450 U/kg、多种钙片0.5 g/kg,补骨制剂Ⅱ高、中、低剂量组分别灌胃给予补骨制剂Ⅱ稠浸膏(剂量以生药量计)12、6、3 g生药/kg,连续给药3个月。末次给药后,检测血清钙(Ca2+)、血清磷(P),超氧化物歧化酶(SOD)、丙二醛(MDA)、血清雌二醇(E2)含量,并测定骨密度、骨生物力学和骨组织形态。结果与去势组相比,低、中、高剂量补骨制剂Ⅱ组在鼠血清中各项检测指标均有显著差异(P0.05),增加腰椎骨密度,提高模型大鼠的股骨最大载荷和刚度,改善骨小梁数量和连续性。结论补骨制剂Ⅱ可明显改善去卵巢大鼠的骨生物力学性能,提高去势大鼠血清中雌激素水平,能防治去卵巢诱导的大鼠骨质疏松,是值得开发的一种中药复方制剂。     

益气活血化瘀法对大鼠促肝癌过程中Fas／FasL影响的研究

目的:探讨益气活血化瘀法对大鼠促肝癌过程中Fas/FasL的影响。方法:160只雄性Wistar大鼠随机分为空白组、模型组、中药高剂量组、中药低剂量组,用二乙基亚硝胺诱导肝癌的发生发展,以益气活血化瘀法对促肝癌大鼠进行治疗,采用酶联免疫法(ELISA)检测肝脏Fas/FasL。结果:与模型组相比,中药高、低剂量组在12、16周时Fas上调,FasL下调。16周时,中药高、低剂量组Fas/FasL的表达差异有显著性意义(P<0.05)。结论:Fas/FasL与肝癌的发生密切相关,益气活血化瘀法通过促进肝脏组织Fas的表达和抑制FasL的表达,从而对减缓大鼠肝癌的形成有一定作用,且呈一定的量效关系。     

淫羊藿总黄酮对去卵巢大鼠骨髓间充质干细胞成骨和成脂分化中DKK1蛋白动态表达的影响

目的观察DKK1在淫羊藿总黄酮调控去势雌性大鼠骨髓间充质干细胞成骨和成脂分化平衡过程中的动态表达,为进一步阐明淫羊藿总黄酮治疗绝经后骨质疏松症的作用机制提供实验依据。方法体外分离培养去势雌性大鼠来源骨髓间充质干细胞,分别在成骨诱导液和脂肪诱导液条件下连续培养15 d,并在此基础上添加剂量为10μg/mL的淫羊藿总黄酮。采用ALP染色、ALP活性测定、油红O染色以及荧光定量PCR技术,观察淫羊藿总黄酮对骨髓间充质干细胞成骨和成脂分化的影响。用酶联免疫法(ELISA)检测淫羊藿总黄酮处理过程中DKK1蛋白的动态表达,观察DKK1蛋白在淫羊藿总黄酮调控去势雌性大鼠骨髓间充质干细胞成骨和成脂分化平衡过程中的作用。结果淫羊藿总黄酮能显著增加骨髓间充质干细胞ALP的表达以及成骨早期分化因子Runx2 mRNA的表达,显著下调骨髓间充质干细胞中脂肪形成关键基因PPARγ-2mRNA的表达,从而抑制脂滴的形成。在成骨诱导条件下,EFs呈时间依赖性下调DKK1的表达;在脂肪诱导条件下,EFs呈时间依赖性抑制DKK1蛋白的上调。结论通过抑制DKK1蛋白的表达调控去势雌性大鼠BMSCs成骨和成脂分化平衡,可能是淫羊藿总黄酮治疗绝经后骨质疏松症的分子机制之一。     

Constitutive expression of the Fas receptor and its ligand in adult human bone marrow: a regulatory feedback loop for the homeostatic control of hematopoiesis

Fas ligand (FasL) mediated apoptosis in the bone marrow may contribute to suppression of hematopoiesis in myelodysplastic syndromes (MDS) and in aplastic anemia, and also to the regulation of normal erythropoiesis. To identify potential effector and target cells in this regulatory pathway, we examined the constitutive expression of Fas receptor (Fas) and FasL (total and cell-surface) in myeloid and lymphoid cells and subsets of CD34+ cells in normal healthy adult human bone marrow using multiparameter flow cytometry. A high proportion of CD34+ cells constitutively expressed cell-surface FasL. However, none of the CD34+ cells expressed Fas alone. A reciprocal gradient of expression of FasL and Fas was observed in subsets of CD34+ cells: as compared to primitive CD34+/HLA-DR(-) (DR(-)) cells, a higher proportion of committed CD34+/HLA-DR(++) (DR(++)) cells expressed FasL but fewer expressed Fas; the expression of both molecules was intermediate in CD34+/HLA-DR(dim) cells. Also, the intensity of FasL expression was higher in DR(++) than in DR(-) cells. These results suggest that the homeostatic regulation of myelopoiesis in normal bone marrow is mediated via an autoregulatory feedback loop by myeloid cells and progenitors themselves, at least partly via the Fas-FasL pathway. This notion is also consistent with our recent observation that overexpression of FasL by myeloid cells in MDS correlates directly with anemia, transfusion requirements, and shorter survival, an example of dysregulation of this pathway.     

Expression of Fas and Fas-ligand in donor hematopoietic stem and progenitor cells is dissociated from the sensitivity to apoptosis

OBJECTIVE: The interaction between the Fas receptor and its cognate ligand (FasL) has been implicated in the mutual suppression of donor and host hematopoietic cells after transplantation. Following the observation of deficient early engraftment of Fas and FasL-defective donor cells and recipients, we determined the role of the Fas-FasL interaction. METHODS: Donor cells were recovered after syngeneic (CD45.1-->CD45.2) transplants from various organs and assessed for expression of Fas/FasL in reference to lineage markers, carboxyfluorescein succinimidyl ester dilution, Sca-1 and c-kit expression. Na?ve and bone marrow-homed cells were challenged for apoptosis ex vivo. RESULTS: The Fas receptor and ligand were markedly upregulated to 40% to 60% (p < 0.001 vs 5-10% in na?ve cells) within 2 days after syngeneic transplantation, while residual host cells displayed modest and delayed upregulation of these molecules ( approximately 10%). All lin(-)Sca(+)c-kit(+) cells were Fas(+)FasL(+), including 95% of Sca-1(+) and 30% of c-kit(+) cells. Fas and FasL expression varied in donor cells that homed to bone marrow, spleen, liver and lung, and was induced by interaction with the stroma, irradiation, cell cycling, and differentiation. Bone marrow-homed donor cells challenged with supralethal doses of FasL were insensitive to apoptosis (3.2% +/- 1% vs 38% +/- 5% in na?ve bone marrow cells), and engraftment was not affected by pretransplantation exposure of donor cells to an apoptotic challenge with FasL. CONCLUSION: There was no evidence of Fas-mediated suppression of donor and host cell activity after transplantation. Resistance to Fas-mediated apoptosis evolves as a functional characteristic of hematopoietic reconstituting stem and progenitor cells, providing them competitive engraftment advantage over committed progenitors.     

Estrogens up-regulate the Fas/FasL apoptotic pathway in lactotropes

The Fas/FasL system provides the major apoptotic mechanism for many cell types, participating in cell turnover in hormone-dependent tissues. In the present study, we localized both Fas and FasL in anterior pituitary cells, mainly in lactotropes and somatotropes. The percentage of anterior pituitary cells showing immunoreactivity for Fas or FasL was higher in cells from rats killed in proestrus than in diestrus. Also, the proportion of pituitary cells from ovariectomized (OVX) rats expressing Fas or FasL increased in the presence of 17beta-estradiol (10(-9) M). This steroid increased the percentage of lactotropes with immunoreactivity for Fas or FasL and the percentage of somatotropes expressing Fas. Activation of Fas by an agonist anti-Fas antibody (Mab-Fas) decreased the vi-ability-3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT assay)-of anterior pituitary cells from OVX rats cultured in the presence of 17beta-estradiol. Also, membrane-bound FasL decreased cell viability-[3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium] assay (MTS assay)-only when anterior pituitary cells from OVX rats were incubated with 17beta-estradiol. Moreover, FasL increased the percentage of hypodiploid anterior pituitary cells (flow cytometry). Mab-Fas increased the percentage of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling (TUNEL)-positive pituitary cells and lactotropes from OVX rats only when cells were incubated in the presence of 17beta-estradiol. Also, Mab-Fas triggered apoptosis of anterior pituitary cells from rats killed at proestrus but not at diestrus. Our results show that 17beta-estradiol up-regulates the expression of the Fas/FasL system in anterior pituitary cells and increases Fas-induced apoptosis in lactotropes, suggesting that Fas-induced apoptosis could be involved in the pituitary cell renewal during the estrous cycle.     

雌二醇对大鼠成骨细胞凋亡受体mRNA表达的影响

目的建立成骨细胞体外培养模型，并研究雌二醇（E2）对体外培养大鼠成骨细胞主要凋亡受体mRNA的调节作用，探讨E2抑制成骨细胞凋亡的机制。方法用新生大鼠颅盖骨进行成骨细胞的原代培养并进行纯化和鉴定；应用TNF-α（200U／ml）以及TNF-α＋E2（10^-8mol／L）进行刺激；用AO-EB染色观察成骨细胞凋亡并计数和计算凋亡率；应用RT—PCR的方法测定成骨细胞的Fas、FasL、TNFR1、TNFR2 mRNA的相对表达量。结果10^-8mol／L的E2明显抑制由TNF-α诱导的成骨细胞Fas、TNFR1 mRNA的表达（P〈0．01），但是对FasL、TNFR2 mRNA的表达没有影响（P〉0．05）。结论雌激素可以通过调节成骨细胞凋亡受体的表达来改变成骨细胞对致死性细胞因子如TNF-α．和FasL等的凋亡敏感性，从而抑制其凋亡。选择性抑制成骨细胞凋亡受体的表达可能有助于增加成骨。     

仙灵骨葆改善骨质疏松大鼠股骨骨生物力学性能的作用及机制研究

目的探讨补肾中药仙灵骨葆对去卵巢骨质疏松模型大鼠皮质骨(股骨)生物力学性能的作用及其相关的机制。方法将40只10月龄wistar雌性大鼠随机分为仙灵骨葆组、倍美力组、正常组和模型组,每组10只。正常组做假手术,其余3组做卵巢切除术。术后正常饲养90 d。第91天开始,仙灵骨葆组、倍美力组分别给予临床等效剂量相应药物:仙灵骨葆55 mg/d(胶囊量),倍美力0.01 mg/d,正常组和模型组不给药。连续给药90 d后处死大鼠,测定股骨的几何尺寸、极惯性矩、抗扭截面模数、截面惯性矩、抗弯截面模数、骨矿密度和股骨的生物力学试验。结果模型大鼠股骨干外径变细,骨皮质面积减少,抗弯、抗扭截面模数变小,骨矿密度减损;股骨的生物力学性能明显下降,骨强度降低。用药组大鼠股骨干外径增粗,骨皮质面积增加,抗弯、抗扭截面模数增大,骨矿密度提高。股骨的生物力学性能明显改善,骨强度增加。结论仙灵骨葆能够提高股骨宏观结构的生物力学应答调节功能,使股骨干外径增粗,皮质骨面积增加,骨丢失减少使股骨结构的抗弯、抗扭截面模数增大,使骨的力学结构优化,骨强度提高。     

A role for the Fas/Fas ligand apoptotic pathway in regulating myeloid progenitor cell kinetics

Bone marrow from wild-type mice and mice with mutated Fas (lpr) or mutated Fas ligand (gld) was used to investigate the role of the Fas/FasL system in the regulation of myeloid progenitor cell kinetics.Granulocyte-macrophage colony-forming cells (CFU-GM) were measured by a standard colony assay and the proliferative activity of CFU-GM was measured by replating primary colonies and observing secondary colony formation. Fas expression was restored to lpr mouse bone marrow cells by retrovirus-mediated gene transfer and gld mouse marrow cells were treated with soluble FasL. Wild-type marrow cells were treated with YVAD (a caspase inhibitor) or anti-Fas monoclonal antibodies.There were greater frequencies of myeloid progenitor cells (CFU-GM) in lpr and gld mouse marrow compared to wild-type (WT) marrow (p = 0.0008). The proliferative capacity of CFU-GM was also significantly greater for lpr and gld CFU-GM compared to WT CFU-GM (p = 0.0003 and 0.0001, respectively). Retrovirus-mediated restoration of Fas into lpr marrow, and provision of soluble FasL (sFasL) to gld CFU-GM reduced CFU-GM proliferation to WT levels. Treatment of WT CFU-GM with YVAD or anti-FasL monoclonal antibody increased CFU-GM proliferation to the levels found in lpr and gld CFU-GM. YVAD significantly increased and anti-Fas significantly reduced the proliferative capacity of human CFU-GM (p = 0.015 and 0.04, respectively).Fas, FasL, and caspase activation may play an important role in regulating myeloid progenitor cell kinetics.     

Fas-mediated apoptosis with normal expression of bcl-2 and p53 in lymphocytes from aplastic anaemia

In order to investigate the involvement of apoptosis in the pathogenesis of aplastic anaemia (AA) we measured the expression of the Fas receptor (membrane protein that triggers apoptosis), Fas ligand (FasL), bcl-2 (cytoplasmatic protein that blocks apoptosis) and p53 (nuclear protein that induces apoptosis) in CD3 and CD19 lymphocytes from the peripheral blood or bone marrow of controls, patients with AA, aplastic anaemia in complete remission (AA-CR) and multiply transfused patients without aplastic anaemia. The Fas receptor was overexpressed in both T and B lymphocytes from the peripheral blood and bone marrow from patients with AA. These abnormalities were not detected in AA-CR or multiply transfused patients. CD3/FasL cells were not increased and no FasL expression was detected in B lymphocytes. Bcl-2 was highly expressed in lymphocytes from controls, AA, AA-CR and multiply transfused patients (> 99% of positive cells) whereas p53 was not detected in any group. To further characterize the functional activity of the Fas receptor we performed a Fas-induced apoptosis assay in peripheral blood lymphocytes using an anti-Fas monoclonal antibody. The crosslinking of the Fas receptor transduced an increased apoptotic signal in lymphocytes from AA patients, but not in lymphocytes from controls, AA-CR patients or multiply transfused patients. Taken together, these data suggest that a Fas-based mediated apoptosis without the apparent participation of bcl-2 or p53 is a possible mechanism of lymphocyte depletion in patients with AA. In addition, these findings suggest that Fas expression is a continuous event occurring from progenitor bone marrow cells to mature cells.     

Clinical significance of expression of apoptotic signal proteins in gastric carcinoma tissue

AIM: To evaluate the expressions of apoptotic signal proteins FADD, TRADD, FasL, Fas, and NFκB in gastric carcinoma tissues and their clinical significance. METHODS: Western blot immune trace method was adopted to detect the expressions of apoptotic signal proteins FADD, TRADD, FasL, Fas, and NFκB in 55 tissue specimens of gastric carcinoma. RESULTS: Five apoptotic signal proteins had different expressions in the gastric carcinoma samples and their expressions were not correlated to age (P= 0.085). Expressions of the FADD, FasL, Fas, and NFkB proteins reduced with increase of the volume of tumor with the exception of increased expression the TRADD protein (64.7-71.1%, P= 0.031). With gradual increase of the malignancy of gastric carcinoma tissues, expressions of the FADD, FasL, and Fas proteins decreased (78.6-28.0%, P= 0.008; 78.6-65.9%, P= 0.071; 100.0-46.3%, P= 0.014), while expressions of the TRADD and NFkB proteins increased (42.9-78.1%, P= 0.063; 78.6-79.1%, P= 0.134). With gradual increase of serum CEA, expression of the FADD protein decreased (62.5-34.0%, P = 0.073), but expressions of the TRADD, FasL, Fas, and NFκB proteins increased (0.0-80.8%, P=0.005; 62.5-70.2%, P= 0.093; 0.0-70.2%, P=0.003; 62.5-80.9%, P= 0.075). When compared to the tissues of gastric carcinoma without metastasis, the positive rate of expressions of the FADD and FasL proteins increased, whereas expressions of the TRADD, FADD, and NFkB proteins decreased. There was no significant difference between them (P= 0.095). CONCLUSION: Gastric carcinoma is endurable to Fas-related apoptosis and apoptotic signal proteins are differently expressed in gastric carcinoma.