丹参对血小板源生长因子刺激血管平滑肌细胞增生的影响

目的：研究丹参对血小板源生长因子（PDGF）刺激血管平滑肌细胞（SMC）增生的影响。方法：体外培养大鼠动脉SMC，设对照组、丹参组（3个浓度组：2.0mg/ml，0.4mg/ml，0.08mg/ml）、PDGF组（10ng/ml）及PDGF(10ng/ml)加丹参（3个浓度，同上）组，测定各组SMC数量^H-TdR掺入量。结果：PDGF可刺激SMC数量及^3H-TdR掺入明显增加，分别为基础状态的3倍和2.5倍；丹参呈剂量依赖性地抑制基础状态及PDGF刺激下SMC数量及^3H-TdR掺入的增加。结论：丹参可抑制基础状态及PDGF作用下血管SMC的增生。     

重组人胰岛素样生长因子Ⅰ对大鼠成骨细胞增殖、凋亡及Ⅰ型胶原蛋白合成的影响

目的 观察胰岛素样生长因子Ⅰ（IGF-Ⅰ）对体外培养的大鼠成骨细胞的增殖、凋亡及Ⅰ型胶原蛋白合成的影响，探讨IGF-Ⅰ对骨代谢影响的可能机制。方法 不同浓度rhIGF-Ⅰ刺激体外培养的大鼠成骨细胞，采用噻唑蓝（MTT）法测定细胞增殖能力；肿瘤坏死因子α（TNF-α单独或与rhIGF-Ⅰ共同刺激成骨细胞，流式细胞仪检测细胞周期和凋亡率；rhIGF-Ⅰ刺激成骨细胞，免疫细胞化学结合计算机图像分析系统检测Ⅰ型胶原蛋白的表达。结果 一定浓度IGF-Ⅰ能明显增加成骨细胞数量（P〈0．05），在0．1～100ng／ml这种作用与IGF-Ⅰ的浓度呈正相关；TNF-α在0．1～100ng/ml浓度范围内呈剂量依赖性地促进成骨细胞凋亡（P〈0．05），并使S期细胞减少（P〈0．05），而IGF-Ⅰ能抑制，TNF-α对成骨细胞的促凋亡作用（P〈0．05）；经IGF-Ⅰ的刺激，成骨细胞Ⅰ型胶原蛋白的表达明显高于对照组（P〈0．05）。结论 IGF-Ⅰ对大鼠成骨细胞有明显的促增殖作用，在0．1～100ng/ml之间呈浓度依赖性，IGF-Ⅰ能抑制，TNF-α诱导的大鼠成骨细胞凋亡，IGF-Ⅰ能促进大鼠成骨细胞Ⅰ型胶原蛋白的合成。     

rhBMP-2诱导脂肪成体干细胞向成骨细胞分化的量效作用

目的 探讨体外条件下rhBMP-2诱导脂肪成体干细胞(adipose-derived adult stem cells,ADASCs)向成骨细胞分化和增殖的情况,并观察其量效关系.方法 从成年兔颈后部获取脂肪组织,采用酶消化法分离并培养脂肪成体干细胞.稳定传代后,用不同浓度rhBMP-2对ADASCs进行诱导分化,采用碱性磷酸酶染色及Ⅰ型胶原免疫组织化学染色进行成骨细胞鉴定,采用碱性磷酸酶活性测定及MTT比色法进行分化和增殖活性比较.结果 碱性磷酸酶及Ⅰ型胶原免疫组织化学染色为阳性;当rhBMP-2浓度在100～400 ng/ml时,各组碱性磷酸酶活性提高明显(P＜0.05),在400 ng/ml以上各组则无明显差异(P＞0.05);当rhBMP-2浓度在800 ng/ml以下时,各组增殖活性无明显差异(P＞0.05),在800 ng/ml以上则存在明显的抑制作用,各组存在明显差异(P＜0.05).结论 研究表明,在体外条件下rhBMP-2能诱导脂肪来源干细胞向成骨细胞分化;并且当其浓度在400～800 ng/ml时,能促进脂肪来源干细胞的增殖和分化.     

胰岛素样生长因子-1对成骨细胞生长影响的实验研究

目的:探讨胰岛素样生长因子-1对成骨细胞生长增殖的影响.方法:采用酶消化法获取兔骨膜成骨细胞,取第三代成骨细胞与0.1ng/ml、1ng/ml、10ng/ml的胰岛素样生长因子-1共同体外培养,在第1～7d观察细胞的形态、生长特点,MTT法测定细胞增殖情况,并通过细胞计数绘制细胞生长曲线.结果:不同浓度的胰岛素样生长因子-1对成骨细胞的生长增殖与对照组比较均有显著性差异(P＜0.01),各浓度之间对成骨细胞的生长增殖亦存在显著性差异(P＜0.05).结论:胰岛素样生长因子-1对成骨细胞生长增殖具有促进作用,在0.1～10ng/ml范围内此种作用与浓度呈正相关.     

吲哚昔芬对大鼠成骨细胞增殖和Ⅰ型胶原合成的影响

目的研究吲哚昔芬对大鼠成骨细胞增殖和Ⅰ型胶原合成的影响。方法分离、培养大鼠头盖骨成骨细胞,分别采用四唑盐(MTT)比色实验和3H-Proline(3氢-脯氨酸)法测定成骨细胞增殖和Ⅰ型胶原合成的情况。结果吲哚昔芬作用大鼠成骨细胞48、72h,1×10-10 mol/L吲哚昔芬与对照组比较,MTTA490nm值显著升高(P<0.05),1×10-9、1×10-8 mol/L的吲哚昔芬使MTTA490nm值进一步升高(P<0.01)。经1×10-10 mol/L吲哚昔芬作用72、96h,3H-Proline掺入值显著升高(P<0.05),1×10-9、1×10-8 mol/L的吲哚昔芬使3H-Proline掺入值进一步升高(P<0.05)。分别用1×10-10 mol/L吲哚昔芬和雌二醇作用大鼠成骨细胞72h,二者的MTTA490nm值和3H-Proline掺入值均显著高于对照组,且吲哚昔芬MTTA490nm值和3H-Proline掺入值显著高于雌二醇(P<0.05)。结论吲哚昔芬发挥抗骨质疏松作用在短期主要促进成骨细胞增殖,中期既促进成骨细胞增殖又促进Ⅰ型胶原合成,而长期效应主要是通过促进胶原合成实现,并且其效应显著强于雌二醇,提示吲哚昔芬对骨质疏松的防治作用可能优于雌二醇。     

胰岛素样生长因子-1(IGF-1)对成骨细胞的成骨影响

目的：探讨不同浓度IGF－1对兔成骨细胞的成骨影响。方法：采用组织块细胞培养技术获得兔成骨细胞，第2代成骨细胞分别在含0.1ng/ml,1ng/ml,10ng/ml,20ng/mlIGF－1的DMEM中培养，24，36h后行MTT法检测细胞增殖情况，72，108h收集培养上清进行骨钙素放射免疫法（RI）测定。结果：IGF－1与成骨细胞培养24，36h，经MTT法检测，不同浓度IGF－1与对照组比较，有显著性差异（P＜0．001）；IGF－1浓度为0．1、1、10ng/ml，各组之间相比存在显著性差异（P＜0．05）；IGF－1与成骨细胞培养72．108h，经RI检测，不同浓度IGF－1对成骨细胞合成骨钙素与对照组比较无显著性差异（P＞0．05）：结论：IGF－1对成骨细胞有明显促进增殖作用，在0．1－10ng/ml范围，存在浓度依赖性，未发现IGF－1对成骨细胞合成骨钙素有影响。     

胰岛素样生长因子-1对成骨细胞生长影响的实验研究

目的探讨胰岛素样生长因子-1对成骨细胞生长增殖的影响.方法采用酶消化法获取兔骨膜成骨细胞,取第三代成骨细胞与0.1ng/ml、1ng/ml、10ng/ml的胰岛素样生长因子-1共同体外培养,在第1～7d观察细胞的形态、生长特点,MTT法测定细胞增殖情况,并通过细胞计数绘制细胞生长曲线.结果不同浓度的胰岛素样生长因子-1对成骨细胞的生长增殖与对照组比较均有显著性差异(P＜0.01),各浓度之间对成骨细胞的生长增殖亦存在显著性差异(P＜0.05).结论胰岛素样生长因子-1对成骨细胞生长增殖具有促进作用,在0.1～10ng/ml范围内此种作用与浓度呈正相关.     

血管紧张素Ⅱ对转化生长因子β诱导的人皮肤成纤维细胞增殖的影响

目的 观察血管紧张素Ⅱ(angiotensin Ⅱ,Ang Ⅱ)对人皮肤成纤维细胞增殖及对转化生长因子β(transforming growth factor β,TGF-β)诱导的成纤维细胞增殖作用的影响,并初步探讨可能的信号机制. 方法 取自愿捐献的正常皮肤组织标本,采用胶原酶法行成纤维细胞培养.取第4～5代细胞,按实验设计分别加入不同浓度的Ang Ⅱ(1×10-10、1×10-9、1×10-8、1×10-7 mol/L)、 TGF-β(0.1、1.0、10.0 ng/ml)、1×10-10 mol/L Ang Ⅱ+ 0.1 ng/ml TGF-β共8组;对照组仅加入等量DMEM.以3H-TdR掺入法测定细胞增殖,Western blot法检测抗细胞外信号调节激酶(extracellular signal-regulated kinases,ERK)活性变化,观察不同浓度的Ang Ⅱ或/和TGF-β对培养的成纤维细胞3H-TdR掺入量和ERK磷酸化的影响. 结果 与对照组比较Ang Ⅱ(1×10-9、1×10-8、1×10-7 mol/L)或TGF-β(1.0、10.0 ng/ml)均能促进成纤维细胞的3H-TdR掺入量(P＜0.05);1×10-10 mol/L Ang Ⅱ或0.1 ng/ml TGF-β单独使用不影响成纤维细胞的3H-TdR掺入量,但二者联合使用提高了成纤维细胞的3H-TdR掺入量(P＜0.05).1×10-7 mol/L Ang Ⅱ、10.0 ng/ml TGF-β增加皮肤成纤维细胞的ERK磷酸化,与对照组比较差异有统计学意义(P＜0.01).1×10-10 mol/L Ang Ⅱ或0.1 ng/ml TGF-β单独刺激成纤维细胞并未影响ERK磷酸化,而二者联合使用增加ERK磷酸化,与对照组比较差异有统计学意义(P＜0.05).应用抗ERK抗体显示各组ERK含量一致. 结论 Ang Ⅱ不仅能作为促有丝分裂素直接促进成纤维细胞分裂增殖,同时也可作为调节因子促进TGF-β的促增殖作用.Ang Ⅱ和TGF-β通过各自特异性受体共同作用于ERK,使磷酸化增加是其产生协同作用可能的机制之一.     

血管紧张素对转化生长因子β诱导的人皮肤成纤维细胞增殖的影响

目的观察血管紧张素(angiotensin,Ang)对人皮肤成纤维细胞增殖及对转化生长因子β(transforminggrowthfactorβ,TGF-β)诱导的成纤维细胞增殖作用的影响,并初步探讨可能的信号机制。方法取自愿捐献的正常皮肤组织标本,采用胶原酶法行成纤维细胞培养。取第4~5代细胞,按实验设计分别加入不同浓度的Ang(1×10-10、1×10-9、1×10-8、1×10-7mol/L)、TGF-β(0.1、1.0、10.0ng/ml)、1×10-10mol/LAng+0.1ng/mlTGF-β共8组;对照组仅加入等量DMEM。以3H-TdR掺入法测定细胞增殖,Westernblot法检测抗细胞外信号调节激酶(extracellularsignal-regulatedkinases,ERK)活性变化,观察不同浓度的Ang或/和TGF-β对培养的成纤维细胞3H-TdR掺入量和ERK磷酸化的影响。结果与对照组比较Ang(1×10-9、1×10-8、1×10-7mol/L)或TGF-β(1.0、10.0ng/ml)均能促进成纤维细胞的3H-TdR掺入量(P<0.05);1×10-10mol/LAng或0.1ng/mlTGF-β单独使用不影响成纤维细胞的3H-TdR掺入量,但二者联合使用提高了成纤维细胞的3H-TdR掺入量(P<0.05)。1×10-7mol/LAng、10.0ng/mlTGF-β增加皮肤成纤维细胞的ERK磷酸化,与对照组比较差异有统计学意义(P<0.01)。1×10-10mol/LAng或0.1ng/mlTGF-β单独刺激成纤维细胞并未影响ERK磷酸化,而二者联合使用增加ERK磷酸化,与对照组比较差异有统计学意义(P<0.05)。应用抗ERK抗体显示各组ERK含量一致。结论Ang不仅能作为促有丝分裂素直接促进成纤维细胞分裂增殖,同时也可作为调节因子促进TGF-β的促增殖作用。Ang和TGF-β通过各自特异性受体共同作用于ERK,使磷酸化增加是其产生协同作用可能的机制之一。     

男性老年性骨质疏松患者血清IGF-Ⅰ测定及临床意义

目的探讨胰岛素样生长因子-Ⅰ(IGF-Ⅰ)与男性老年性骨质疏松的关系.方法对26例老年骨质疏松男性患者和28例男性对照者行IGF-Ⅰ等生化指标测定,同时测定骨密度.结果老年男性骨质疏松患者腰椎和左股骨颈骨密度显著低于对照组(P＜0.001;P＜0.001);血清IGF-Ⅰ水平明显低于对照组(80.40±17.41)ng/mL与(157.82±28.80)ng/mL(P＜0.001),而血钙、血磷和碱性磷酸酶(ALP)水平在两组间差异无显著性.对照组和骨质疏松组腰椎、左股骨颈骨密度均与血清IGF-Ⅰ水平高度相关(对照组:r=0.455,P＜0.05;r=0.493,P＜0.01;骨质疏松组:r=0.529,P＜0.01;r=0.657,P＜0.01),而与血钙、血磷、ALP水平无关.结论 IGF-Ⅰ水平与骨质含量具有良好的相关性.IGF-Ⅰ水平测定可作为诊断男性老年性骨质疏松的一项指标.     

Growth potential of different zones of the growth plate—an experimental study in rabbits

Despite clinical efforts to treat growth disturbances only little is known about the growth potential of the different zones of the growth plate. The aim of this study was to investigate the growth potential of different zones of the growth plate. A total of 20 New Zealand White rabbits were used for this experiment. The right and left ulna of each animal were used resulting in a total of 40 ulnae. Animals were assigned into five groups. In groups I and II resection of the metaphyseal (n = 12) or the epiphyseal (n = 6) segment of the growth plate was performed. In group III resection of the growth plate and re‐implantation was performed (n = 6). In group IV the growth plate was resected and re‐implanted after a 180° rotation (n = 6). Animals in group V served as controls. Histologic and radiologic examinations were performed to evaluate the growth process at 1, 2, 4, and 12 weeks following surgery. In group I, III, and IV temporary growth disturbance which was compensated within a short time was observed. Resection of the epiphyseal part resulted in growth arrest of the distal ulna in combination with normal growth of the radius which led to and valgus deformity of the limb. The results of this study indicate the importance of the reserve zone for the functioning of the growth plate. © 2011 Orthopaedic Research Society Published by Wiley Periodicals, Inc. J Orthop Res 30:162–168, 2012     

Age and pattern of the onset of differential growth among growth plates in rats

Differential growth is the phenomenon whereby growth plates in the same individual at the same time all have uniquely different axial growth velocities. Differential growth is clearly present in the adolescent skeleton. In this study we ask two questions. When and by what pattern does the phenomenon of differential growth begin? Second, to what extent are the development of differential growth velocities correlated with changes in hypertrophic chondrocyte volume and/or with changes in chondrocytic production/turnover? Four growth plates (proximal and distal radial; proximal and distal tibial) were studied at 24 different time points in Long‐Evans rats between the 17th gestational day (when differential growth does not exist) and postnatal day 27 (when differential growth is well established). Growth velocities were measured using fluorochrome labeling. Using stereological methodology, multiple chondrocytic kinetic parameters were measured for all growth plates. Elongation of the proximal radial growth plate decreases relative to elongation in the other three growth plates in the late fetal phase. Differential growth is fully expressed at postnatal day 13 when the other three growth plates start to decrease daily elongation at different rates. Differential growth is primarily associated with differences in hypertrophic cell volume manifested when growth deceleration occurs. This study also illustrates that differential growth is superimposed on systemic regulators that affect all growth plates simultaneously. The most dramatic illustration of this is the sharp decline in growth velocity in all four growth plates that occurs perinatally. © 2008 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 26:1457–1465, 2008     

Compensatory renal growth: Interactions of nephrectomy serum and urine antisera leading to a new theory of renal growth regulation

Summary Compensatory renal growth is mediated by a substance(s) found in the serum and in urine called renotropin. The interaction of nephrectomy serum and urine antisera upon compensatory renal growth was investigated by administering rat uninephrectomy serum and sham serum and urine to rabbits. The rabbit antisera was given intravenously to uninephrectomy and sham operated rats and kidney weight/body weight ratios were calculated. Antisera against sham serum and urine induced kidney growth as well as antisera aginst uninephrectomy serum and urine given to sham animals. These results suggest the presence of a circulating antigenic inhibitor to kidney growth and suggest that renotropin is made up of a inhibitory as well as a stimulatory substance.     

Subtotal nephrectomy: a mosaic of growth factors

We have studied the distribution of immunoreactive growth factors,by an avidin-biotin-peroxidase technique, throughout the courseof progressive renal scarring in rats submitted to extensiverenal ablation. Groups of rats (n=6) were sacrificed at Days7, 15, 21, 30, 90 and 150 following subtotal nephrectomy (SNx)by ligation and resection of the renal poles. During the earlystages, when compensatory renal growth took place, increasedrenal immuno staining for insulin-like growth factor-I (IGF-I)and epidermal growth factor (EGF) was detected within the collectingducts and distal tubules, respectively. As renal scarring becameestablished by Days 90 and 150, these two growth factors weredetected within the cells of damaged and vacuolated distal tubules.By contrast, a progressive increase immunostain for platelet-derivedgrowth factor (PDGF)-AB was apparent within the glomeruli fromDay 15 onward preceding the onset of glomerulosclerosis. A thirdstaining pattern was apparent by Day 15 for transforming growthfactor-ß (TGF ß) and by Day 30 for IGF-Iconsisting of a perivascular and interstitial distribution coincidingwith adventitial expansion and tubulo-interstitial fibrosis,respectively. A mosaic of growth factors is expressed withinthe kidneys of rats submitted to extensive renal ablation.     

Changes in gene expression of growth factors and their receptors during castration-induced involution and androgen-induced regrowth of rat prostates

To find candidates for the mediator of the growth-promoting action of androgen in rat prostates, the changes in the steady-state levels of mRNAs coding for several growth factors and their receptors were examined by Northern blot analysis during castration-induced involution, and subsequent regrowth induced by androgen in the ventral and dorsolateral lobes. The changes in the growth factor systems and a typical secretory protein in the ventral lobe were similar to, but more prominent than, those in the dorsolateral lobe, showing the higher androgen dependency of the ventral lobe. Among the growth factors and their receptors investigated, only epidermal growth factor (EGF) showed apparent positive androgen dependency: EGF mRNA content in the ventral lobe decreased to about 30% of the normal level within 24 hr after castration, and increased, attaining about 200–300% of the normal level 3–5 days after androgen administration to castrated rats. mRNAs coding for all other factors examined, i.e., transforming growth factor-α (TGF-α), EGF receptor, basic fibroblast growth factor (bFGF), keratinocyte growth factor (KGF), FGF receptor 1, TGF-β1, TGF-β type II receptor, hepatocyte growth factor (HGF), and c-MET/HGF receptor, increased after castration in greater or lesser degree, and after a brief pause or a decrease some of them increased again attaining a second peak 3–5 days after androgen replacement. The second increase was evident in TGF-α, EGF receptor, KGF, and c-MET mRNAs. These results indicate the possibility that multiple growth factor-receptor systems participate in the androgen-dependent regrowth of castrated rat prostates. © 1996 Wiley-Liss, Inc.     

Modulation of the microenvironment by growth factors regulates the in vivo growth of skeletal myoblasts

OBJECTIVES

To investigate the optimal microenvironment for efficient myoblast transplantation in vivo.

MATERIALS AND METHODS

The effects of co‐culture with growth factors, including basic fibroblast growth factor (bFGF), hepatocyte growth factor (HGF), insulin‐like growth factor‐I) and platelet‐derived growth factor (PDGF), on in vitro growth, migration and proteolytic activity of mouse skeletal myoblasts were investigated. Myoblasts were co‐injected with growth factors into the subcutis and bladder wall of nude mice, and its impact on the growth patterns of myoblasts in vivo assessed.

RESULTS

There was dose‐dependent stimulation of in vitro myoblast growth after treatment with each of the four growth factors, but bFGF induced the most marked increase in the growth of myoblasts. Treatment of myoblasts with all types of growth factors also resulted in a dose‐dependent increase in the in vitro migration of myoblasts, and PDGF had the most prominent effect on myoblast migration. Increased secretion of matrix metalloproteinase‐9 (MMP‐9) in myoblasts induced by growth factors was proportional to their increased migration capacity, which was partly inhibited by SB‐3CT, an inhibitor of MMP‐9. The in vivo growth of myoblasts was significantly enhanced by co‐injection with all types of growth factor into both the subcutis and bladder wall, but this effect was most marked 1 and 2 weeks after co‐injection with bFGF and PDGF, respectively. Furthermore, there was synergistic in vivo growth of myoblasts by co‐injection of both bFGF and PDGF compared with that achieved with either agent alone.

CONCLUSIONS

These findings suggest that modulation of the microenvironment using growth factors, particularly bFGF and PDGF, could provide the optimum condition for effective myoblast transplantation in vivo.     

Effects of unilateral arterial infusion of GH and IGF-I on tibial longitudinal bone growth in hypophysectomized rats

Summary We have studied the effect of local arterial infusion of bacterially produced human growth hormone (hGH), insulinlike growth factor I (IGF-I), or pituitary-derived ovine prolactin (oPRL) on longitudinal bone growth of hypophysectomized rats. The substances were infused during a 14-day period by osmotic mini-pumps through a catheter which was implanted into the femoral artery of one hindlimb. Longitudinal bone growth was measured by the intravital marker tetracycline. Infusion of 1 μg hGH per day stimulated bone growth only of the treated limb and not of the uninfused contralateral limb. Infusion of 10 μg hGH per day also stimulated unilateral longitudinal bone growth, but the uninfused contralateral limb also showed a significant growth response, probably because local administration of GH at this dose caused a significant elevation of GH in the systemic circulation. As a result, the differential growth response between the GH-treated and untreated limbs decreased compared to rats that were infused with 1 μg hGH per day. Unilateral arterial infusion of 5 μg human IGF-I or 10 μg oPRL per day did not produce a significant growth response. The results of the present study confirm the observation by Schlechter and co-workers [9, 16], who demonstrated that unilateral arterial infusion of GH maintained tibial cartilage width following hypophysectomy in the rat. The results of Schlechter and co-workers and the results of the present study show that GHin vivo stimulates epiphyseal cartilage growth directly. However, an increased local production of insulinlike growth factors is probably of importance for the expression of the direct effect of GH on longitudinal bone growth. The present results do not completely rule out the possibility that insulinlike growth factors in the circulation might have the growth plate as a target organ.     

胰岛素和胰岛素样生长因子及其结合蛋白与结直肠癌发生的关系

目的 探讨血清胰岛素、胰岛素样生长因子(IGF-1)、IGF结合蛋白(IGFBPs)及体质量指数(BMI)、腰臀围比(WHR)的变化及与结直肠癌发生、发展的关系.方法 检测对象为2006年6月至2007年10月间住院收治和门诊复查的结直肠癌患者615例(术前检测244例,术后371例)和健康对照者150例.采用酶联免疫吸附法检测血清胰岛素、IGF-1和IGFBPS水平.结果 结直肠癌患者术前血清胰岛素、IGF-1水平和IGF-Ⅰ/IGFBP-3比值与健康对照组、术后患者比较,均明显升高,IGFBP-3水平明显降低,差异均有统计学意义(P<0.05,P<0.01).结直肠癌术后未发生转移者与有肝或腹腔远处转移者胰岛素、IGF-1、IGFBP-1、IGFBP-3、IGF-1/IGFBP-3比较.差异均无统计学意义(P>0.05).结直肠癌患者WHR明显高于健康对照组(P<0.01和P<0.05):而BMI与健康对照组比较,差异无统计学意义(P>0.05).结肠癌患者WHR、BMI与胰岛素水平、IGF-1/IGFBP-3比值呈正相关(P<0.01,P<0.05),与IGFBP-3呈负相关(P<0.01,P<0.05);直肠癌患者WHR与血清瘦素、胰岛素水平及BMI与血清IGFBP-1水平均呈正相关(P<0.05),与其他无相关性(P>0.05).结论 胰岛素、IGF-1水平和IGF-Ⅰ/IGFBP-3比值升高及IGFBP-3水平降低,可能与结直肠癌的发生有关,但与肿瘤转移与否无关,中心性肥胖是结肠癌发生的危险因素之一.     

胰岛素和胰岛素样生长因子及其结合蛋白与结直肠癌发生的关系

目的 探讨血清胰岛素、胰岛素样生长因子(IGF-1)、IGF结合蛋白(IGFBPs)及体质量指数(BMI)、腰臀围比(WHR)的变化及与结直肠癌发生、发展的关系.方法 检测对象为2006年6月至2007年10月间住院收治和门诊复查的结直肠癌患者615例(术前检测244例,术后371例)和健康对照者150例.采用酶联免疫吸附法检测血清胰岛素、IGF-1和IGFBPS水平.结果 结直肠癌患者术前血清胰岛素、IGF-1水平和IGF-Ⅰ/IGFBP-3比值与健康对照组、术后患者比较,均明显升高,IGFBP-3水平明显降低,差异均有统计学意义(P<0.05,P<0.01).结直肠癌术后未发生转移者与有肝或腹腔远处转移者胰岛素、IGF-1、IGFBP-1、IGFBP-3、IGF-1/IGFBP-3比较.差异均无统计学意义(P>0.05).结直肠癌患者WHR明显高于健康对照组(P<0.01和P<0.05):而BMI与健康对照组比较,差异无统计学意义(P>0.05).结肠癌患者WHR、BMI与胰岛素水平、IGF-1/IGFBP-3比值呈正相关(P<0.01,P<0.05),与IGFBP-3呈负相关(P<0.01,P<0.05);直肠癌患者WHR与血清瘦素、胰岛素水平及BMI与血清IGFBP-1水平均呈正相关(P<0.05),与其他无相关性(P>0.05).结论 胰岛素、IGF-1水平和IGF-Ⅰ/IGFBP-3比值升高及IGFBP-3水平降低,可能与结直肠癌的发生有关,但与肿瘤转移与否无关,中心性肥胖是结肠癌发生的危险因素之一.     

胰岛素和胰岛素样生长因子及其结合蛋白与结直肠癌发生的关系

目的 探讨血清胰岛素、胰岛素样生长因子(IGF-1)、IGF结合蛋白(IGFBPs)及体质量指数(BMI)、腰臀围比(WHR)的变化及与结直肠癌发生、发展的关系.方法 检测对象为2006年6月至2007年10月间住院收治和门诊复查的结直肠癌患者615例(术前检测244例,术后371例)和健康对照者150例.采用酶联免疫吸附法检测血清胰岛素、IGF-1和IGFBPS水平.结果 结直肠癌患者术前血清胰岛素、IGF-1水平和IGF-Ⅰ/IGFBP-3比值与健康对照组、术后患者比较,均明显升高,IGFBP-3水平明显降低,差异均有统计学意义(P<0.05,P<0.01).结直肠癌术后未发生转移者与有肝或腹腔远处转移者胰岛素、IGF-1、IGFBP-1、IGFBP-3、IGF-1/IGFBP-3比较.差异均无统计学意义(P>0.05).结直肠癌患者WHR明显高于健康对照组(P<0.01和P<0.05):而BMI与健康对照组比较,差异无统计学意义(P>0.05).结肠癌患者WHR、BMI与胰岛素水平、IGF-1/IGFBP-3比值呈正相关(P<0.01,P<0.05),与IGFBP-3呈负相关(P<0.01,P<0.05);直肠癌患者WHR与血清瘦素、胰岛素水平及BMI与血清IGFBP-1水平均呈正相关(P<0.05),与其他无相关性(P>0.05).结论 胰岛素、IGF-1水平和IGF-Ⅰ/IGFBP-3比值升高及IGFBP-3水平降低,可能与结直肠癌的发生有关,但与肿瘤转移与否无关,中心性肥胖是结肠癌发生的危险因素之一.