抑制细胞

结果显示HBV感染患者存在免疫调节功能的紊乱，其中至少包括两类抑制细胞功能低下，并和病情有关。

The results showed that both spontaneous and ConA induced suppression were significantly reduced in patients with HBV infection and the suppressor cell dysfunction correlated well with disease activity .

目的研究溃疡性结肠炎（UC）和克隆病（CD）患者T抑制细胞的活性及其临床意义。

AIM To study on the alterations of T suppressor cell function in patients with ulcerative colitis ( UC ) and Crohn 's disease ( CD ) and their clinical significance .

实验方法：K562/A02耐药性以MTT法检测阿霉素抑制细胞生长作用，计算耐药倍数。

The cell growth inhibition of K5662 / A02 cells was assayed using MTT method .

其中，抑制细胞凋亡的Bcl-2与促进细胞凋亡的Bax是调节中枢。

Among them , inhibiting cell apoptosis Bcl-2 and promoting cell apoptosis Bax are regulating center .

CaM拮抗剂TFP或兔抗CaMγ球蛋白可抑制细胞增殖。

CaM antagonist TFP and anti CaM γ globulin had an inhibitory effect on cell proliferation rate .

原癌基因Bcl一2的蛋白表达产物具有抑制细胞凋亡的效应，其作用与Bax基因的蛋白表达产物相反，Bax过度表达导致细胞凋亡。

The effect of Bcl - 2 is inhibiting apoptosis , and that of Bax is promoting apoptosis .

而NEO可抑制细胞迁移和侵袭，但促进细胞增殖。

While NEO can inhibit cell migration and invasion , but promote cell proliferation .

目的研究创伤对反抑制细胞（Tcs）的影响。方法采用小鼠截肢伤模型，利用长柔毛野豌豆凝集素（VVL）分离获取Tcs细胞，以直接免疫荧光法检测Tcs细胞数目；

Objective Effect of trauma on contrasuppressor T cells ( Tcs )

Bcl-2的过度表达伴Bax的低表达提示可以抑制细胞凋亡而且延长细胞周期，由此延缓肿瘤增殖。

Bcl-2 over-expression with low expression of Bax can inhibit apoptosis , prompt the extension of the cell cycle and thus slow tumor proliferation .

DNA作为目标分子用于识别在抑制细胞功能紊乱和治疗某些疾病中的天然和人工分子，这在无机生物化学中是极其重要的。

Serving as a target molecule , the recognition of DNA for natural and artificial molecules in the inhibition of cellular disorders and in therapy of certain diseases is of paramount importance in inorganic biochemistry .

p53基因是一种抗癌基因，其主要功能是抑制细胞增殖、诱导细胞凋亡和诱导分化。

The p53 gene is a kind of tumor suppressor gene . Its main function is inhibiting cell proliferation , inducing apoptosis and leading to the cell differentiation .

Bcl-2蛋白在出血后一定时间内持续升高，但与细胞凋亡不同步，表明了bcl-2的抑制细胞凋亡的作用。

The expression of Bcl-2 protein keeps increasing during certain period after ICH but not synchronous with apoptosis , indicating that bcl-2 has the effect in inhibiting apoptosis .

MTT结果显示：铜呈剂量依赖性和时间依赖性的抑制细胞生长活力和破坏线粒体整体功能（p＜0.05，p＜0.01）。

MTT results revealed Copper could inhibit the viability of cells and damage the function of mitochondrion in dose and time dependent ( p < 0 . 05 , p < 0 . 01 ) .

PF能降低缺氧复氧损伤所致的细胞内钙离子浓度升高，蛋白激酶C参与其抑制细胞内钙超载，是PF发挥保护作用的细胞内信号转导调节因子。

Propofol attenuated the increasing of intracellular concentration of calcium induced by hypoxia and reoxygenation injury . PKC signaling passway participated in inhibiting the calcium overload and produced protection . 4 .

低浓度的Pae与化疗药物协同可产生较强的抑制细胞增殖作用。

Pae in low concentration had synergetic effect in inhibiting the proliferation of HT-29 cells with several chemotherapy agents .

MTT法显示转染VEGF165基因能促进内皮细胞VEGF蛋白的表达，促进细胞增殖，抑制细胞凋亡。

As revealed in the MTT the transfected VEGF 165 gene could improve the expression of VEGF proteins in EC , accelerate cell proliferation and inhibit the development of apoptosis of EC .

可以抑制细胞外基质成分FN在肾间质的沉积，减少UUO大鼠肾间质纤维化面积，推测其抑制CTGF表达上调的作用可能是其抗肾小管损伤及间质纤维化的作用机制之一。

It is inferred that it may be one of mechanisms of Astragalus and Safflower mixture suppressing renal tubular damage and interstitial fibrosis .

主要结果如下：太阳UVR辐射抑制细胞的光合固碳速率和光化学效率。

The main results are as follows : Solar UVR inhibited the photosynthetic carbon fixation and photochemical efficiency of the cells .

提示PNS抑制细胞Ca~（2+）内流可能是其抗脂质过氧化反应的主要机理之一。

These findings indicate that the inhibition of PNS on the calcium influx might be one of the mechanisms of anti-lipid peroxidation in spinal cord injury in rats .

PTEN过表达能够显著抑制细胞在Fn基质上的活动：细胞在Fn基质上的迁移下降了35%；

It was observed that the overexpression of PTEN gene significantly inhibited cell motility on extracellular matrix ( Fn ), and the cell migration on fibronectin was reduced by 35 % .

结论抗HER2／neu的特异性抗体可能通过抑制细胞的信号传递系统而抑制肿瘤生长。

Therefore , It suggests that the possible mechanism of the inhibition of tumor growth by anti HER2 / neu specific antibody probably through interfering with the activation of signal transduction system .

结论胃癌细胞系SGC-7901中存在胃泌素／CCK-B受体自分泌环，阻断此自分泌环后能抑制细胞增殖，促进细胞凋亡。

Conclusion Human gastric cancer SGC-7901 cells possess the gastrin / the CCK-B receptor autocrine loop . Blocking the autocrine loop inhibits the cell proliferation and promotes the cell apoptosis .

8CPTcAMP可通过影响细胞周期调控蛋白E2F和P21的表达而抑制细胞增殖，并促进As2O3介导的PMLRARα融合蛋白降解。

In addition , 8-CPT-cAMP was able to inhibit the cell growth by modulating the expression of some important cell cycle regulators and to facilitate the As 2O 3-mediated degradation of PML-RAR α fusion protein .

结论ADM、DEX巩膜塞植入体能够明显降低玻璃体中bFGF和PDGF的浓度，抑制细胞过度增生，降低牵拉性视网膜脱离的发生率，从而防治PVR的形成和发展。

Conclusion The ADM and DEX scleral plugs can degrade the concentration of bFGF and PDGF obviously , inhibit excessive proliferation and reduce the incidence rate of tractional retinal detachment , therefore prevent the formation and development of PVR .

MKP1通过对p38的负调控来抑制细胞凋亡，从而增强细胞增殖，改变大津医科大学硕士研究生学位论文了细胞增殖与细胞凋亡之间的平衡，促进前列腺上皮的恶性转化。

MKP , inactivate p38 by an inverse feedback and inhibits cell apoptosis , which accelerate the malignant transformation of prostate epithelium . The disruption of balance between cell proliferation and apoptosis underlies the cell kinetics of genesis and development of prostate cancer .

结论：干扰人神经胶质瘤细胞系U-87细胞的ClC-2基因表达可以抑制细胞的增殖，提示ClC-2基因可能成为控制人恶性胶质瘤生长的新靶点。

CONCLUSION : These results demonstrate that CIC-2 siRNA could inhibit the cell proliferation of a human glioma cell line U-87 , thus ClC-2 gene may be used as a novel target for the suppression of the growth of human malignant glioma cells .

其生物学效应广泛，有明显的舒张血管、降低血压、抑制细胞生长、增殖等功能，在肾脏功能调节方面起着重要的作用。

It is important for regulating renal function .

抑郁症患者T淋巴细胞亚群和T抑制细胞功能研究

A study of T Lymphocyte Subsets and T Suppressor Cell Function in Depressive Patients

反向寡脱氧核苷酸抑制细胞周期素D1表达及对黑素瘤细胞增殖的影响

Antisense Oligodeoxynucleotide Inhibits the Expression of Cyclin D_1 and Its Influence on Growth of Melanoma Cells

褪黑素通过抑制细胞内钙超载，对脂多糖诱导的胎鼠脑细胞损伤有保护作用。

Melatonin has a protective effect on lipopolysaccharide-induced brain cells injury of fetal rat by inhibiting intracellular calcium overload .