锌离子对牙各矿化成份破骨细胞性吸收的体外调控

目的:研究锌离子对破骨细胞体外吸收牙片功能的影响.方法:体外分离、培养新生乳兔破骨细胞,与玻片和灭活牙片共同培养,加入不同浓度锌离子.抗酒石酸酸性磷酸酶(TRAP)染色鉴定玻片上的破骨细胞,显微摄影分析破骨细胞吸收造成的牙片上的吸收陷窝,原子吸收分光光度法测定溶出的钙,并将实验组与对照组上清液钙离子浓度的比值定义为骨吸收指数,以评价破骨细胞的功能.结果:体外成功分离培养出多核的、TRAP(+)的破骨细胞.破骨细胞吸收牙片时,首先在接近牙根牙骨质或牙本质部位开始形成吸收陷窝,这与这些部位的矿化程度相对较低有关;破骨细胞在牙片上形成的吸收陷窝与骨片相比,吸收陷窝数量较少,体积较小,多为正圆形;吸收深度较浅,常为大面积的浅吸收.用原子吸收分光光度法测定不同浓度的锌离子对溶出的钙和骨吸收指数的影响,初步结果表明,培养第3天,1×10^-4～1×10^-14 mol/L锌离子刺激破骨细胞吸收牙片,其中1×10^-8 mol/L,1×10^-10 mol/L和1×10^-14 mol/L锌离子能够显著刺激吸收(P＜0.05);但是到了培养第7天,各浓度组除了对照组和1×10-14 mol/L锌离子还进一步有吸收外,其余浓度锌离子组的上清液钙离子浓度与自身第3天相比都有降低,但与同时期的对照组相比差异无统计学意义.在培养末期(第7天)1×10^-4～1×10^-7 mol/L,1×10^-9 mol/L,1×10^-12 mol/L和1×10^-13 mol/L浓度组的骨吸收指数小于1,而1×10^-8 mol/L,1×10^-10 mol/L,1×10^-11 mol/L和1×10^-14 mol/L浓度组骨吸收指数都大于1.结论:锌离子对破骨细胞吸收功能的作用与浓度和时程有关.     

紫杉醇和吉西他滨对激素非依赖性前列腺癌的作用

OBJECTIVE: To observe the synergistic effects of paclitaxel (PA) and gemcitabine (GE) in vitro and in vivo on prostate cancer cell line PC-3. METHODS: Cell morphological observation, MTT assay, flow cytometry, and immunocytochemical method were used to observe the effects of 1+/-10(-6) mol/L, 1 x 10(-7) mol/L and 1 x 10(-8) mol/L PA and 1 x 10(-7) mol/L, 1 x 10(-8) mol/L and 1 x 10(-9) mol/L GE on prostate cancer cell line PC-3 in vitro in a single or combined administration for 48 h. Male BALB/C-nu mice bearing PC-3 prostate cancer were treated with docetaxol and retinoic acid singly or synergistically, followed by measurement of the body weight and immunohistochemical examination of serum prostate specific antigen (PSA) and PSA expression in the implanted tumors. RESULTS: GE at the concentration of 1 x 10(-8) mol/L significantly enhanced the effect of PA above 1 x 10(-7) mol/L in inducing growth inhibition (with an inhibition rate over 50.8%+/-4.2%, P<0.05) and apoptosis (apoptosis rate over 22.9%+/-2.3%, P<0.05) of PC-3 cells and in down-regulating the expression of cyclin D1 (expression rate no higher than 9.6%+/-1.6%, P<0.01) in PC-3 cells. GE lowered the rate of PA-induced cell cycle arrest at G(2)/M phase from 70.3%+/-9.7% to 38.2%+/-4.2%, and partially reversed the G(2)/M arrest (P<0.01). Synergistic treatment of the tumor-bearing mice caused little change in the body weight, but the serum PSA (51+/-14 ng/ml), implanted tumor mass (3.2+/-0.5 g) and PSA expression in the tumors (30%+/-3.7%) were all decreased significantly in comparison with the control mice (21.6+/-1.7 g). CONCLUSIONS: GE can enhance PA-induced tumor cell growth suppression and apoptosis in a synergistic manner both in vitro and in vivo, suggesting their great potential in clinical treatment of androgen-independent prostate cancer.     

血管紧张素Ⅱ对肝癌细胞增殖的影响及其机制研究

目的:研究血管紧张素Ⅱ对肝癌HepG2细胞增殖的影响及其机制.方法:采用CCK-8法测定不同浓度血管紧张素Ⅱ作用24、48 h对HepG2细胞增殖的影响.通过蛋白质免疫印迹法测定血管紧张素Ⅱ处理后HepG2细胞内细胞外信号调节激酶(ERK)1/2和血管紧张素Ⅱ-1型受体(AT1R)蛋白表达水平.结果:作用24 h,10...     

Dexamethasone-induced adipogenesis in primary marrow stromal cell cultures: mechanism of steroid-induced osteonecrosis

Background In steroid-induced osteonecrosis, hypertrophy and hyperplasia of marrow fat cells and lipid deposition of osteocytes can be found in the femoral head. However, the precise reason is not clear yet. The aim of this study was to observe the effect of dexamethasone （Dex） on differentiation of marrow stromal cells （MSCs）, and to investigate the pathobiological mechanism of steroid-induced osteonecrosis. Methods MSCs in cultures were treated with increasing concentrations of Dex （0, 10^-9, 10^-8, 10^-7, and 10^-6 mol/L） continuously for 21 days. The cells, which were exposed to 0 mol/L （control） or 10^-7 mol/L Dex for 4-21 days, were then cultured for 21 days without Dex. MSCs were stained with Sudan Ⅲ. Number of adipocytes was counted under a light microscope. The activity of alkaline phosphatase （ALP） of MSCs treated with 0, 10^-8, 10-7, and 10^-6 mol/L Dex for 12 days, and that treated with 0 mol/L and 10^-7 mol/L Dex for 8, 10, or 12 days were determined. The levels of triglycerides, osteocalcin and cell proliferation of MSCs treated with 0 mol/L and 10^-7 mol/L Dex were detected. The mRNA expression levels of adipose-specific 422（aP2） gene and osteogenic gene type I collagen in MSCs treated with 0 mol/L and 10^-7 mol/L Dex for 6 days were analyzed by whole-cell dot-blot hybridization. Statistical analysis was performed using Student＇s t test and analysis of variance. P values less than 0.05 were considered significant statistically. Results The number of adipocytes in cultures increased with the duration of MSCs＇ exposure to Dex and the concentration of Dex. The level of ALP activity in the MSCs decreased with concentration of Dex. In the control group, it was 8.69 times of that in the 10^-7 mol/L Dex group on day 12 （t=20.51, P〈0.001）. The level of triglycerides in 10^-7 mol/L Dex group was 3.40 times of that in the control （t=11.00, P〈0.001）. The levels of cell proliferation and osteocalcin in the control were 1.54 and 2.42 times of that in the 10^-7 mol/L Dex group respectively. As compared to the control, the mRNA expression of adipose-specific 422（aP2） gene in 10^-7mol/L Dex group was significantly increased （t=36.48, P〈0.001）, and that of osteogenic gene type I collagen was decreased （t=42.07, P〈0.001）. Conclusions Dex can directly induce the differentiation of MSCs into a large number of adipocytes and inhibit their osteogenic differentiation, which provide a novel explanation for the pathologic changes of steroid-induced osteonecrosis.     

选择性环氧合酶-2抑制剂对胃癌细胞生长的影响

目的　观察选择性环氧合酶 - 2 ( COX- 2 )抑制剂 (美洛昔康、塞来昔布、罗非昔布 )对人胃癌细胞株SGC790 1生长的影响以及罗非昔布对人胃癌裸鼠移植瘤生长的抑制效应。方法　采用 3H-胸腺嘧啶核苷 ( 3H- Td R)掺入法了解细胞的增殖 ;用免疫组化检测细胞增殖核抗原 ( PCNA)及细胞 COX- 2的表达 ;用 TUNEL 染色法检测细胞凋亡。建立人胃癌裸鼠原位移植瘤模型 ,给予罗非昔布 8周 ,观察肿瘤大小、COX- 2及 PCNA表达情况。结果三种选择性 COX- 2抑制剂均较阿司匹林更有效抑制体外培养的胃癌细胞 3H- Td R掺入 ,3H-胸腺嘧啶掺入值与药物浓度呈负相关。美洛昔康、塞来昔布、罗非昔布对胃癌细胞 3H-胸腺嘧啶掺入的 IC50 分别为 1.18× 10 - 7mol/ L、1.68× 10 - 8mol/ L、4.3 9× 10 - 9mol/ L。经 1× 10 - 5m ol/ L 的上述三种药物作用 2 4h,SGC790 1细胞凋亡指数分别为 19.8%± 1.8%、2 4.6%± 1.2 % 3 1.2 %± 2 .2 %。 COX- 2抑制剂的选择性越高 ,凋亡指数也显著升高 ( P<0 .0 1)。罗非昔布对裸鼠胃癌原位移植瘤的抑瘤率为 93 .9% ;肿瘤组织的 COX- 2、PCNA表达均较对照组明显下降。结论　COX- 2抑制剂的选择性越高 ,对胃癌生长抑制作用越强。罗非昔布可成为胃癌综合治疗的重要药物之一     

Effects of Nitric Oxide on Proliferation and Apoptosis of Cultured Bovine Trabecular Meshwork Cell

Nitric Oxide (NO) shows a dualism in thepathogenesis of glaucoma:in one side,NO can im-prove outflow facility of aqueous humor and dropintraocular pressure (IOP) ;on the other side,ithas direct toxic effect on retinal ganglion cell[1] .Our preveious studies demonstrated,in some ex-tent,pressure could induce inducible nitric oxidesynthase(i NOS) m RNA expression,so to increase NOS synthesis and NO level[2 ] .In this experimentwe discussed the effects of NO on the proliferationand apopto…     

阿托伐他汀对骨髓来源的成骨细胞中OPG mRNA/RANKL mRNA水平的影响

目的:观察阿托伐他汀对体外培养骨髓基质细胞来源的成骨细胞中OPGmRNA/RANKLmRNA表达的影响。方法:小鼠骨髓基质细胞在成骨条件培养基中传代培养,加入不同浓度的阿托伐他汀。通过半定量RT鄄PCR的方法,比较不同浓度药物影响下OPGmRNA和RANKLmRNA表达的变化,评判阿托伐他汀对这两种蛋白表达的影响作用。结果:半定量RT鄄PCR的观察显示在传代培养7天时各组均有OPGmRNA的转录,随着药物浓度的增加,mRNA转录水平逐渐增加,10-6mol/L组和10-7mol/L组明显高于对照组(P<0.05)。RANKLmRNA水平随着药物浓度的增加呈现出下降的现象,10-6mol/L组和10-7mol/L组明显低于对照组。结论:在小鼠骨髓基质细胞来源的成骨细胞中,阿托伐他汀促进了成骨细胞OPG的表达,同时能抑制细胞RANKL的表达。     

多西紫杉醇和维甲酸对前列腺癌PC-3细胞的协同作用

目的　观察多西紫杉醇和维甲酸对前列腺癌细胞系 PC- 3的体外体内协同作用 ,并探讨其可能的作用机制。方法　应用光镜形态学 ,四甲基噻唑蓝 (MTT)法 ,流式细胞仪和免疫细胞化学法观察 10 - 6、10 - 7、10 - 8mol/L 多西紫杉醇和 10 - 5、 10 - 6、10 - 7mol/L 维甲酸在体外单药或协同对前列腺癌细胞系 PC- 3的生长抑制作用、诱导凋亡、对细胞 DNA含量及 Cyclin D1 表达的影响。观察 PC- 3细胞荷瘤裸鼠单独及协同使用多西紫杉醇和维甲酸前后的体质量、肿瘤重量、血清 PSA和肿瘤 PSA免疫组化表达的变化。结果　 10 - 6 mol/L和 10 - 5mol/L维甲酸协同 10 - 7mol/L以上多西紫杉醇作用 4 8h,可增强对前列腺癌 PC- 3细胞的生长抑制作用 (抑制率≥ 6 9.2 % ,P<0 .0 1) ,增强诱导凋亡作用 (凋亡率≥ 2 3.8% ,P<0 .0 5 ) ,下调 Cyclin D1 的表达 (表达率≤ 14 .2 % ) ,与阳性对照组Cyclin D1 表达率 2 5 .5 %相比差异有显著性 (P<0 .0 5 )。维甲酸使多西紫杉醇所致的 G2 /M期细胞比例由 74 .3%变为 5 7.8% ,部分地逆转了其 G2 /M期细胞周期阻滞 (P<0 .0 5 )。协同治疗前后裸鼠体质量无明显变化 ,但肿瘤质量〔(2 .8± 0 .4 ) g〕、血清 PSA〔(4 3± 11) ng/ml〕和肿瘤 PSA免疫组化的表达率〔(2 6± 3.2 ) %〕在协     

In vitro inhibitory effect of CD_8~ cells from patients with aplastic anemia on normal CFU-GM growth was blocked by cimetidine

ＩｎｖｉｔｒｏｉｎｈｉｂｉｔｏｒｙｅｆｅｃｔｏｆＣＤ＋８ｃｅｌｓｆｒｏｍｐａｔｉｅｎｔｓｗｉｔｈａｐｌａｓｔｉｃａｎｅｍｉａｏｎｎｏｒｍａｌＣＦＵＧＭｇｒｏｗｔｈｗａｓｂｌｏｃｋｅｄｂｙｃｉｍｅｔｉｄｉｎｅＷａｎｇＭｉｎｇｃｈｕｎ汪明春，ＹａｎｇＬ...     

芒果苷元对TGF-β1诱导的HK-2细胞EMT的影响

  目的  研究芒果苷元对TGF-β1诱导的HK-2细胞EMT的影响。  方法  MTT法检测各浓度芒果苷元对HK-2细胞活力的影响；用TGF-β1诱导HK-2细胞成EMT模型，并给以芒果苷元干预，在TGF-β1诱导24 h时显微镜下拍照记录细胞形态变化，划痕实验法检测细胞迁移能力，Transwell法检测细胞侵袭能力，Western blot法检测纤连蛋白（fibronectin，FN）和Ⅰ型胶原（collagen type Ⅰ，Col Ⅰ）蛋白表达水平。  结果  （1）芒果苷元（10-9～10-5 mol/L）浓度下HK-2细胞活力均无明显变化（P > 0.05）；（2）与正常组相比，模型组细胞形态变长变梭，迁移和侵袭能力显著增强（P < 0.05，0.01），FN和ColⅠ蛋白表达水平显著上调（P < 0.05，0.01）；与模型组相比，芒果苷元组细胞能维持原来的鹅卵石形，迁移和侵袭能力显著下降（P < 0.05，0.01），FN和ColⅠ蛋白表达水平显著下调（P < 0.05）。  结论  芒果苷元能抑制TGF-β1诱导的HK-2细胞迁移和侵袭，阻止细胞形态的改变，下调细胞外基质成分FN和ColⅠ的蛋白表达，从而抑制EMT的发展。     

四环素—哌嗪雌酚酮对小鼠骺板I型胶原表达的影响

目的：研究四环素－哌嗪雌酚酮（XW630）对胚胎小鼠骺板I型胶原的表达的影响。方法：采用胚胎小鼠体外培养模型，通过免疫组织化学手段，观察XW630对I型胶原蛋白表达水平的影响。结果：当培养基中XW630浓度为10^-7mol/L和10^-8mol/L时，各区I型胶原蛋白免疫组织化学染色阳性细胞面积与对照组相比均显著增加；与同浓度的雌酚酮组相比，106-7mol/L XW630组增殖区和肥大区阳性细胞面积增加。当浓度降至10^-9mol/L，只有肥大区阳性细胞面积增加。随浓度升高，各区阳性细胞面积呈增加趋势。结论：在体外培养条件下，XW630剂量依赖地上调小鼠骺板静止区、增殖区和肥大区I型胶原蛋白的表达水平。     

Graft-versus-leukemia effects from donor lymphocyte infusion after nonmyeloablative allogeneic bone marrow transplantation in mice

Background Nonmyeloablative allogeneic bone marrow transplantation has been used since the 1990s as a new hematological stem cell transplantation strategy for treating hematological diseases. The purpose of this study was to explore the graft-versus-leukemia (GVL) effects of donor lymphocyte infusions (DLIs) after nonmyeloablative allogeneic bone marrow transplantations, while assessing the declines in treatment-associated morbidity, mortality, and graft-versus-host disease (GVHD).Methods A total of 615 (H-2k) mice were injected with L615 tumor cells and received 500 cGy (60Coγ-ray) irradiation three days later, followed by an allogeneic bone marrow transplantation (allo-BMT). The allo-grafts consisted of 3×10（7） bone marrow cells and 1×10（7） spleen cells from BALB/C (H-2d) donor mice. Two days after the allo-BMT, the recipient mice were given 200 mg/kg of cyclophosphamide. Subsequently, recipient mice were infused with either donor spleen cells ［2×10（7）］ on day 14 or 21, or donor spleen cells ［5×10（7）］ pretreated with hydrocortisone and cyclosporin A (CsA) in vitro on day 14 post-BMT.Results The median survival time of mice that received DLI on day 21 and pretreated DLI on day 14 post-BMT was longer than that of controls and the day 14 DLI group (P&lt;0.01). No evidence of severe GVHD was observed in the day 21 DLI group nor in the day 14 treated DLI group. Mixed chimerism was confirmed in the day 14 DLI group, the day 14 treated DLI group, and the day 21 DLI group on the thirteenth day post-transplantation; full donor chimerism was observed two weeks after DLI.Conclusion Donor lymphocyte infusion after nonmyeloablative bone marrow transplantation may reduce transplantation-associated morbidity and mortality while strengthening graft-versus-leukemia effects.     

阿托品对人视网膜色素上皮细胞D407株 表达及分泌TGF β2的调控

目的：通过观察不同浓度阿托品联合10-5 mol/L卡巴胆碱干预下D407细胞表达及分泌TGF β2的变化,探讨阿托品对RPE细胞表达及分泌TGF β2的调控作用。方法：常规培养D407细胞,药物干预前换用无血清培养基培养, 分为4组。（1）实验组（A组）：A1~A5组依次加入10-4～10-8 mol/L阿托品,孵育30 min后每组加入10-5 mol/L卡巴胆碱;（2）阴性对照组（B组）：B1~B5组依次加入10-4～10-8 mol/L阿托品;（3）阳性对照组（C组）：加入10-5 mol/L卡巴胆碱;（4）空白对照组（D组）：不加药物。干预24 h后采用RT PCR,Western印迹及ELISA法检测细胞胞浆中TGF β2 mRNA及蛋白质的表达水平及上清液中TGF β2的含量。统计学方法采用单因素方差分析。结果：实验组D407细胞胞浆TGF β2 mRNA和蛋白质表达水平及上清中TGF β2蛋白质含量均较阳性对照组低,10-4 mol/L阿托品可完全阻断10-5 mol/L卡巴胆碱上调TGF β2表达及分泌的作用,其效应具有浓度依赖性（F=1 056.897, 1 320.170, 475.657;P＜0.001）。阴性对照组D407细胞胞浆TGF β2 mRNA和蛋白质表达水平及上清中TGF β2蛋白质含量与空白对照组比较差异无统计学意义（P＞0.05）。结论：阿托品可有效抑制卡巴胆碱促进人RPE细胞表达及分泌TGF β2的功能,提示M受体参与介导此过程。     

孕酮对脂肪细胞促酰化蛋白受体和下游信号蛋白表达的作用

目的 观察孕酮对3T3-L1(前)脂肪细胞促酰化蛋白(ASP)受体C5L2 mRNA和细胞表面C5L2蛋白表达的影响,以及孕酮对ASP下游信号蛋白的作用.方法 体外培养3T3-L1细胞,诱导细胞分化,不同浓度孕酮作用于3T3-L1(前)脂肪细胞,孵育过夜后收获细胞,分别采用RT-PCR和流式细胞仪检测ASP受体mRNA和蛋白表达情况;采用Western印迹法检测基础状态和ASP激发后Gαq/11,Gβ,p-PKCα和p-PKCζ蛋白表达.结果 孕酮最大抑制成熟脂肪细胞14% C5L2 mRNA (P＞0.05)和蛋白表达22%(36%±15%vs 46%±12%,P＜0.01),高浓度孕酮(1 × 10-6 mol/L)能显著性抑制前脂肪细胞66%C5L2 mRNA(0.17±0.11 vs 0.50±0.18,P＜0.01)和29%C5L2蛋白表达(36%±16%vs 51%±20%,P＜0.05).高浓度孕酮在一定程度上抑制ASP激发后成熟脂肪细胞Gαq/11,Gβ,p-PKCα和p-PKCζ的表达,各蛋白表达分别减少了41%(0.71±0.21 vs 1.20 ±0.24,P＜0.05),63%(0.55±0.32 vs 1.48±0.40,P＜0.05),49%(0.53±0.20 vs 1.04 ±0.19,P＜0.01)和32%(0.36 ±0.10 vs 0.53 ±0.20,P＞0.05).在前脂肪细胞,高浓度孕酮显著性抑制ASP刺激的59%Gαq/11(0.42 ±0.18 vs 1.04±0.28,P＜0.01),43%Gβ(0.77 ±0.09 vs 1.35 ±0.27,P＜0.05),51%p-PKCα(0.44 ±0.15 vs 0.90 ±0.25,P＜0.05)和30%p-PKCζ(0.27±0.08vs 0.39±0.12,P＜0.05)蛋白表达.结论 孕酮诱导ASP抵抗的发生,ASP抵抗参与了高浓度孕酮引起的脂肪细胞胰岛素抵抗状态的病理生理过程.     

Effects of angiotensin II and losartan on the growth and proliferation of hepatic stellate cells.

OBJECTIVE: To investigate the effects of angiotensin II (AngII) and AT1a blocker losartan on growth and proliferation of rat hepatic stellate cells (HSCs). METHODS: Rat HSCs were isolated, cultured and identified, followed by incubation with AngII or losartan at different concentrations. The cell growth and proliferation were assessed via cell counting and MTT assay, and the effects of the agents on HSC DNA synthesis evaluated by way of (3)H-thymidine incorporation ((3)H-TDR). RESULTS: AngII (1 x 10(-9) to 1 x 10(-7) mol/L) stimulated HSC proliferation as demonstrated by cell counting, MTT assay and thymidine incorporation test (P < 0.05), but such effect was not observed at lower doses (<1 x 10(-9) mol/L). Losartan had significant inhibitory effect on HSC growth at the concentration of 1 x 10(-8) to 1 x 10(-6) mol/L (P < 0.05), but not at lower doses (<1 x 10(-8) mol/L). Co-stimulation of the cells with losartan and AngII did not result in a significant increase in cell number as compared with the control group (P > 0.05). CONCLUSION: Rapid proliferation of rat HSCs occurs in response to AngII treatment, but is inhibited after AT1a receptor is blocked with the antagonist losartan.     

对-壬基酚对MCF-7人类乳腺癌细胞雌激素受体表达的影响

目的　观察对 -壬基酚 (p- NP)对 MCF- 7人类乳腺癌细胞株雌激素受体 (ER)及 ERαm RNA表达的影响 ,探讨其雌激素样活性。方法　以 RPMI 16 4 0培养液 (含 10 %小牛血清 )对 MCF- 7细胞进行半开放式贴壁培养 ,试验前以 DMEM(不含酚红 )培养液洗涤细胞 ,以含 3% C/D胎牛血清的 DMEM(不含酚红 )培养液继续培养 3d。试验设溶剂对照、阳性对照和 p- NP 5个浓度组 ,采用免疫组织化学法和定量 RT- PCR法分别对 MCF- 7细胞 ER蛋白和 ERαm RNA表达情况进行分析。结果　 1× 10 - 5m ol/L p- NP作用于 MCF- 7细胞 2 4 h下调 ER蛋白表达 ;1× 10 - 6 mol/L～ 1× 10 - 5m ol/L p- NP作用于 MCF- 7细胞 2 h和 2 4 h下调 ERαm RNA表达。p- NP各浓度组均表现出 ER蛋白和 ERαm RNA表达随 p- NP作用于 MCF- 7细胞时间的延长而进一步下降的趋势。结论　 p- NP可模拟雌激素下调 MCF- 7细胞 ER蛋白和 ERαm RNA表达 ,具有雌激素样活性     

亲溶酶体剂——十二烷基吗啡啉对白血病骨髓净化的实验研究

亲溶酶体剂——十二烷基吗啡啉(N-dodecyl morpholine,NDM)体外对小鼠白血病L_(7811)细胞系细胞有明显的杀灭作用,其100％杀死10~6个/mlL_(7811)细胞浓度为15mg/ml。用此浓度NDM处理含5％L_(7811)细胞的615小鼠骨髓细胞后回输给615小鼠,对照组存活天数为16.3±1.78d,溶剂组为15.8士2.32d,而NDM处理组可长期存活(>40d)。615小鼠在接受致死剂量(800rad)照射后输注经NDM处理的含5％L_(7811)细胞的615小鼠骨髓细胞,小鼠不死于白血病而死于放射病,当输注细胞数加倍时,小鼠存活期从8.75土1.13d延长到10.68±0.99d(P<0.01)。     

尼尔雌醇和左炔诺孕酮对人成骨肉瘤 MG-63细胞株雌激素受体亚型的作用

目的：观察不同浓度的尼尔雌醇(NYL)和左炔诺孕酮(LNG)对人成骨肉瘤MG-63细胞株ERα和ERβ表达的作用，探讨旁分泌效应对ERα和ERβ基因表达的影响。方法：人成骨肉瘤MG-63细胞株分为（1）空白对照组：用含1% BSA无血清MEM培养液培养48 h；（2）阳性对照组：培养液中加入10-8 mol/L的17β-estradiol (E2) 培养48 h；（3）药物处理组：培养液中分别加入10-10，10-8，10-6 mol/L的NYL或LNG培养48 h；（4）药物处理+换液组：培养液中分别加入10-10 mol/L的NYL或10-8 mol/L LNG培养48 h，每12 h更换新的含有相应药物的培养液。用半定量RT-PCR检测各组细胞ERα和ERβmRNA的表达。结果：NYL及LNG均能诱导ERα和ERβ亚型mRNA表达上调，诱导ERαmRNA表达的最强作用浓度均为10-6 mol/L。NYL，LNG对ERβ mRNA表达最强作用浓度分别为10-10，10-8 mol/L。每12 h更换干预培养液对ERα表达无影响，但可抑制ERβ的表达。结论：NYL和LNG均可诱导MG-63细胞株ERα和ERβ mRNA表达上调，且2种亚型的表达存在相互制约关系；在NYL和LNG诱导ER亚型表达上调过程中ERβ的表达可能受到旁分泌作用的影响。     

地塞米松抑制培养牛眼小梁细胞AQP1表达

目的测定地塞米松对体外培养牛眼小梁细胞水通道蛋白-1(aquaporin1,AQP1)表达的影响,探讨糖皮质激素性青光眼房水引流阻力的形成机制。方法将传3代的牛眼小梁细胞用数字表法随机分为对照和地塞米松处理组。将不同浓度的地塞米松(10-5、10-6、10-7mol/L)分别加入培养液持续培养14 d,免疫细胞化学方法检测小梁细胞AQP1表达水平,计算机图像分析软件测量细胞表面积。结果经不同浓度地塞米松处理后的小梁细胞AQP1表达量吸光度值A显著低于对照组(均P=0.000)。10-7mol/L地塞米松作用下细胞表面积显著大于对照组,而10-6mol/L和10-5mol/L地塞米松作用下细胞表面积显著低于对照组(均P=0.000)。结论地塞米松抑制牛眼小梁细胞AQP1表达,可能参与了糖皮质激素性青光眼的发生。