Curcumin Inhibits Prostate Cancer Bone Metastasis by Up-Regulating Bone Morphogenic Protein-7 <i>in Vivo</i>

A number of studies have focused on the beneficial properties of Curcumin (diferuloyl methane, used in South Asian cuisine and traditional medicine) such as the chemoprevention of cancer. Recent studies have also indicated that this material has significant benefits for the treatment of cancer and is currently undergoing several clinical trials. We have been interested in the application of this compound as a therapeutic agent for advanced prostate cancer, particularly the skeletal complications in this malignancy. Our earlier work indicated that this compound could inhibit the osteomimetic properties which occur in castration resistant prostate cancer cells, by interfering with the common denominators between these cancer cells and the bone cells in the metastatic tumor microenvironment, namely the osteoblasts and the osteoclast. We predicted that curcumin could break the vicious cycle of reciprocal stimulation that results in uncontrolled osteolysis in the bony matrix. In this work, we have evaluated the potential of this compound in inhibiting the bone metastasis of hormone refractory prostate cancer cells in an established animal model. Our results strongly suggest that curcumin modulates the TGF-βsignaling that occurs due to bone matrix degradation by up-regulating the metastasis inhibitory bone morphogenic protein-7 (BMP-7). This enhancement of BMP-7 in the context of TGF-β in the tumor microenvironment is shown to enhance the mesenchymal-to-epithelial transition. Most importantly, we show that as a result of BMP-7 up-regulation, a novel brown/beige adipogenic differentiation program is also up-regulated which plays a role in the inhibition of bone metastasis. Our results suggest that curcumin may subvert the TGF-β signaling to an alternative adipogenic differentiation program in addition to the previously established interference with the osteomimetic properties, thus inhibiting the bone metastatic processes in a chemopreventive as well as therapeutic setting.

Effects of exogenous recombinant human bone morphogenic protein-7 on the corneal epithelial mesenchymal transition and fibrosis

AIM：To evaluate the effect of exogenous recombinant human bone morphogenic protein-7（rhBMP-7）on transforming growth factor-β（TGF-β）-induced epithelial mesenchymal cell transition（EMT）and assessed its antifibrotic effect via topical application.METHODS：The cytotoxic effect of rhBMP-7 was evaluated and the EMT of human corneal epithelial cells（HECEs）was induced by TGF-β. HECEs were then cultured in the presence of rhBMP-7 and/or hyaluronic acid（HA）. EMT markers,fibronectin,E-cadherin,α-smooth muscle actin（α-SMA）,and matrix metaloproteinase-9（MMP-9）,were evaluated. The level of corneal fibrosis and the reepithelization rate were evaluated using a rabbit keratectomy model. Expression of α-SMA in keratocytes were quantified following treatment with different concentrations of rhBMP-7.RESULTS：Treatment with rhBMP-7 attenuated TGF-β-induced EMT in HECEs. It significantly attenuated fibronectin secretion（31.6%; P〈0.05）,the α-SMA protein level（72.2%; P〈0.01）,and MMP-9 expression（23.6%,P〈0.05）in HECEs compared with cells grown in the presence of TGF-β alone. E-cadherin expression was significantly enhanced（289.7%; P〈0.01）in the presence of rhBMP-7. Topical application of rhBMP-7 combined with 0.1% HA significantly reduced the amount of α-SMA~＋ cells by 43.18%（P〈0.05）at a concentration of 2.5 μg/mL and by 47.73%（P〈0.05）at 25 μg/mL,compared with the control group,without disturbing corneal reepithelization.CONCLUSION：rhBMP-7 attenuates TGF-β-induced EMT in vitro,and topical application of rhBMP-7 reduces keratocyte myodifferentiation during the early wound healing stages in vivo without hindering reepithelization. Topical rhBMP-7 application as biological eye drops seems to be feasible in diseases involving TGF-β-related corneal fibrosis with corneal reepithelization disorders.

Environmentally adaptive reshaping of plant photomorphogenesis by karrikin and strigolactone signaling

Coordinated morphogenic adaptation of growing plants is critical for their survival and propagation under fluctuating environments.Plant morphogenic responses to light and warm temperatures,termed photomorphogenesis and thermomorphogenesis,respectively,have been extensively studied in recent decades.During photomorphogenesis,plants actively reshape their growth and developmental patterns to cope with changes in light regimes.Accordingly,photomorphogenesis is closely associated with diverse growth hormonal cues.Notably,accumulating evidence indicates that light-directed morphogenesis is profoundly affected by two recently identified phytochemicals,karrikins(KARs)and strigolactones(SLs).KARs and SLs are structurally related butenolides acting as signaling molecules during a variety of developmental steps,including seed germination.Their receptors and signaling mediators have been identified,and associated working mechanisms have been explored using gene-deficient mutants in various plant species.Of particular interest is that the KAR and SL signaling pathways play important roles in environmental responses,among which their linkages with photomorphogenesis are most comprehensively studied during seedling establishment.In this review,we focus on how the phytochemical and light signals converge on the optimization of morphogenic fitness.We also discuss molecular mechanisms underlying the signaling crosstalks with an aim of developing potential ways to improve crop productivity under climate changes.

Three-dimensional bioprinting of multicell-laden scaffolds containing bone morphogenic protein-4 for promoting M2 macrophage polarization and accelerating bone defect repair in diabetes mellitus

Critical-sized bone defect repair in patients with diabetes mellitus remains a challenge in clinical treatment because of dysfunction of macrophage polarization and the inflammatory microenvironment in the bone defect region.Three-dimensional(3D)bioprinted scaffolds loaded with live cells and bioactive factors can improve cell viability and the inflammatory microenvironment and further accelerating bone repair.Here,we used modified bioinks comprising gelatin,gelatin methacryloyl(GelMA),and 4-arm poly(ethylene glycol)acrylate(PEG)to fabricate 3D bioprinted scaffolds containing BMSCs,RAW264.7 macrophages,and BMP-4-loaded mesoporous silica nanoparticles(MSNs).Addition of MSNs effectively improved the mechanical strength of GelMA/gelatin/PEG scaffolds.Moreover,MSNs sustainably released BMP-4 for long-term effectiveness.In 3D bioprinted scaffolds,BMP-4 promoted the polarization of RAW264.7 to M2 macrophages,which secrete anti-inflammatory factors and thereby reduce the levels of pro-inflammatory factors.BMP-4 released from MSNs and BMP-2 secreted from M2 macrophages collectively stimulated the osteogenic differentiation of BMSCs in the 3D bioprinted scaffolds.Furthermore,in calvarial critical-size defect models of diabetic rats,3D bioprinted scaffolds loaded with MSNs/BMP-4 induced M2 macrophage polarization and improved the inflammatory microenvironment.And 3D bioprinted scaffolds with MSNs/BMP-4,BMSCs,and RAW264.7 cells significantly accelerated bone repair.In conclusion,our results indicated that implanting 3D bioprinted scaffolds containing MSNs/BMP-4,BMSCs,and RAW264.7 cells in bone defects may be an effective method for improving diabetic bone repair,owing to the direct effects of BMP-4 on promoting osteogenesis of BMSCs and regulating M2 type macrophage polarization to improve the inflammatory microenvironment and secrete BMP-2.

Bone morphogenic protein signaling in spinal cord injury

Spinal cord injury(SCI)is a debilitating injury that results from traumatic or non-traumatic insults to the spinal cord,causing significant impairment of the patient's activity and quality of life.Bone morphogenic proteins(BMPs)are a group of polyfunctional cytokines belonging to the transforming growth factor beta superfamily that regulates a wide variety of cellular functions in healthy and disease states.Recent studies suggest that dysregulation of BMP signaling is involved in neuronal demyelination and death after traumatic SCI.The focus of this article is to describe our current understanding of the role of BMP signaling in the regulation of cell fate,proliferation,apoptosis,autophagy,and inflammation in traumatic SCI.First,we will describe the expression of BMPs and pattern of BMP signaling before and after traumatic SCI in rodent models and in vitro.Next,we will discuss the role of BMP in the regulation of neuronal and glial cell differentiation,survival,functional recovery from traumatic SCI,and the gap in knowledge in this area that requires further investigation to improve SCI prognosis.

Drosophila embryo syncytial blastoderm cellular architecture and morphogen gradient dynamics： Is there a correlation？

During embryo development in many metazoan animals, the first differentiated cell type to form is anepithelial cell. This epithelial layer is modified by developmental cues of body axes formation to give rise to various tissues. The cells that arise are mesenchymal in nature and are a source of other tissue types. This epithelial to mesenchymal transition is used for tissue type formation and also seen in diseases such as cancer. Here we discuss recent findings on the cellular architecture formation in the Drosophila embryo and how it affects the developmental program of body axes formation. In particular these studies suggest the presence of compartments around each nucleus in a common syncytium. Despite the absence of plasma membrane boundaries, each nucLeus not only has its own endoplasmic reticulum and Golgi complex but also its own compartmentalized plasma membrane domain above it. This architecture is potentially essential for morphogen gradient restriction in the syncytial Drosophila embryo. We discuss various properties of the dorso-ventral and the antero-posterior morphogen gradients in the Drosophila syncytium, which are likely to depend on the syncytial architecture of the embryo.

抑制LncRNA PANDA表达对人心脏瓣膜间质细胞钙化的改善作用及其机制

目的观察抑制长链非编码RNA PANDA(LncRNA PANDA)表达对人心脏瓣膜间质细胞(hVICs)钙化的影响,并探讨其机制是否与核酸转录因子YA(NF-YA)、凋亡相关蛋白Bax、锚定蛋白2(Notch2)、骨形态发生蛋白2(BMP-2)有关。方法将体外培养的hVICs分为三组,正常对照组加入间质细胞培养基+10%胎牛血清,培养7 d;钙化组加入钙化诱导液,培养7 d。PANDA-siRNA组加入钙化诱导液培养3 d后,采用Lipofectamine^(TM)3000转染试剂盒转染PANDA-siRNA,再培养4 d。取各组分组培养7 d的细胞,采用实时荧光定量PCR法检测LncRNA PANDA相对表达量,光学显微镜观察细胞形态,Western blotting法检测NF-YA、Bax、Notch2、BMP-2蛋白相对表达量,ELISA法检测细胞上清液BMP-2水平。结果PANDA-siRNA组、正常对照组、钙化组细胞LncRNA PANDA相对表达量及上清液BMP-2蛋白水平均依次升高,组间两两比较P均<0.05。PANDA-siRNA组细胞结构清晰,呈条索状生长,生长稍缓慢;钙化组细胞成骨样改变,细胞聚集,呈网状结构;正常对照组细胞贴壁生长,生长迅速。与正常对照组比较,钙化组细胞NF-YA、Bax、Notch2、BMP-2蛋白相对表达量均升高,PANDA-siRNA组均降低(P均<0.05)。结论诱导钙化后的hVICs LncRNA PANDA表达升高,抑制LncRNA PANDA表达可减轻其成骨样改变,其机制可能与降低NF-YA、Bax、Notch2、BMP-2表达有关。

机械离心力对成骨细胞骨形态发生蛋白信号通路中Runx-2 mRNA的影响

背景:机械力对成骨细胞生理活动存在一定影响,Runx-2是骨形态发生蛋白信号的靶目标,是调节成骨细胞分化的重要因子,骨形态发生蛋白信号转导通路参与了成骨细胞对机械离心力刺激的生理响应过程。目的:观察不同转速及时间作用下,机械离心力对成骨细胞骨形态发生蛋白信号通路的影响。方法:将MC3T3-E1细胞用含体积分数10%胎牛血清的DMEM培养基预处理24 h后,分为对照组,90 r/min组、180 r/min及250 r/min组,每组再分为离心6,12,24 h亚组,给予不同转速离心力和相同转速不同时间的刺激,重复实验3次。对照组同步置于除离心外相同的环境中。提取总RNA,并反转录为cDNA,通过实时荧光定量PCR检测Runx2基因表达情况。结果与结论:随着加力时间的延长,Runx2 mRNA的表达增加,二者成正相关,转速为180 r/min组的Runx2mRNA表达明显高于90 r/min组和250 r/min组(P<0.01);90 r/min组和250 r/min组Runx2 mRNA的表达均高于对照组(P=0.039),且都随时间延长差异明显。结果可见离心力大小和离心持续时间不同对成骨细胞骨形态发生蛋白信号通路的生理响应不同,该通路在对力学信号引起的信息传递级联反应中起重要作用。

墨兰组织培养中原球茎的形态解剖研究

通过对墨兰 (Cymidiumsinense)组织培养中原球茎外部形态、内部结构的观察研究 ,发现墨兰茎尖组织培养中产生的原球茎和丛生型原球茎虽外形差别较大 ,但内部结构都具有根的典型特征 .芽的分生组织可以在原球茎表层、丛生型原球茎或其顶端发生 .芽的顶端分生组织与随后产生的根的顶端分生组织共同构成胚状结构 ,其形态与种子胚相似 .由于墨兰组培中先后产生的原球茎和丛生型原球茎其内部结构都属典型的根结构 ,故称之为原球茎值得商榷 .此外 。

1α，25双羟维生素D_3对成骨样细胞增殖与分化的影响

采用同位素掺入，细胞周期、细胞化学和扫描电镜等方法观察了１α，２５双羟维生素Ｄ３［１，２５（ＯＨ）２Ｄ３］对人及大鼠成骨样细胞ＯＳ－７３２和ＲＯＳ１７／２．８增殖及分化的影响。结果表明：１，２５（ＯＨ）２Ｄ３对ＯＳ－７３２细胞增殖的抑制作用呈明显的时效和量效关系。在给１０－７ｍｏｌ／Ｌ的１，２５（ＯＨ）２Ｄ３后第４和第６天，对ＯＳ－７３２细胞生长的抑制率分别为４０％和６０％；对ＤＮＡ，ＲＮＡ和蛋白质合成的抑制作用分别为５９％，４１％和２２％。流式细胞计测定结果表明：１，２５（ＯＨ）２Ｄ３使ＤＮＡ合成受阻；扫描电镜显示：１，２５（ＯＨ）２Ｄ３有抑制ＲＯＳ１７／２．８细胞表面微绒毛的作用。此外，细胞化学染色表明：该激素有增加成骨样细胞碱性磷酸酶活性和促进骨形态形成蛋白合成的作用，即刺激骨形成的作用。

可注射型骨修复材料对兔MSC增殖及分化的影响

目的 :观察以纤维蛋白胶为载体的骨修复材料对兔骨髓基质细胞 (marrowstromalcell,MSC)增殖及分化的影响。方法 :采用细胞培养及组织化学等方法对各材料组兔MSC的增殖、碱性磷酸酶 (alkalinephosphase ,ALP)的活性和染色、细胞贴壁率及Ⅰ型胶原表达进行研究。结果 :( 1)各组材料对细胞贴壁率及促增殖作用的影响总体上由强到弱依次是 :对照组 2→实验组→对照组 1[纤维蛋白胶 (fibrinsealant ,FS) ]→对照组 3→单纯对照组 ,差异有显著性 (p <0 .0 5 )。( 2 )各组细胞的Ⅰ型胶原表达水平和ALP活性由强到弱依次是 :实验组→对照组 3→对照组 1→对照组 2→单纯对照组 ,差异有显著性 ( p <0 .0 5 )。结论 :以纤维蛋白胶为载体的注射型骨修复材料可显著促进MSC贴壁率和向成骨细胞方向的分化水平。

以纤维蛋白胶为载体复合BMP和bFGF的注射型骨修复材料诱导异位成骨的实验研究

目的 :了解以纤维蛋白胶 (Fibrinsealant,FS )为载体的注射型骨修复材料异位诱导成骨的作用 ,为其临床的应用提供实验依据。方法 :实验分组为 :实验组b (FS +bFGF+bBMP)、对照组b1(FS +bBMP)、对照组b2 (bBMP)、实验组r (FS +bFGF +rhBMP 2 )、对照组r1(FS +rhBMP)、对照组r2 (rhBMP)、对照组FS及空白对照组。将各组材料注射或植入小鼠肌袋内 ,采用放射学、形态学、碱性磷酸酶 (ALP)检测等方法对其成骨效应进行研究。结果 :在以bBMP为成骨因子的实验区中 ,实验组b具有高效的骨诱导活性 ,其成骨量显著高于对照组b1、对照组b2、对照组FS及空白对照组(P <0 .0 1) ;在以rhBMP 2为成骨因子的实验区中 ,实验组r同样具有高效的骨诱导活性 ,其成骨量也显著高于对照组r1、对照组r2、对照组FS及空白对照组 (P <0 .0 1)。结论 :以FS为载体复合BMP和bFGF的注射型骨修复材料具有高效的骨诱导活性 ,bFGF可明显增强BMP的骨诱导活性。

BMP-2改良纤维蛋白原支架修复软骨缺损的实验研究

目的 :研究骨形态发生蛋白 (bonemorphogenicprotein ,BMP 2 )在构建改良纤维蛋白胶支架软骨膜块修复关节软骨缺损中的作用。方法 :将软骨细胞种植于改良纤维蛋白胶支架上 ,体外培养 ,在培养系统中加入BMP 2 ,观察软骨细胞在支架中的繁殖以及载体降解情况 ;将培养出的软骨膜块植入于动物关节软骨缺损模型中进行定期观测。结果 :改良纤维蛋白原支架可满足组织工程软骨修复需要 ,BMP 2在用于构建膜块修复关节软骨缺损模型中可促进软骨细胞增殖 ,并在植入 12周动物试验中发现与对照组比较在关节软骨缺损修复质量上有显著性差异 (P <0 .0 1)。结论 :BMP 2在改良纤维蛋白胶软骨膜块中可明显促进组织工程软骨膜块构建以及关节软骨缺损的修复。

Bio-oss复合BMP修复牙种植体周围骨缺损的骨组织学定性与定量分析

目的:分析和评价以无机牛骨(deproteinizednaturalbovinemineral, Bio-oss)作为载体材料复合骨形成蛋白(bonemorphogenicprotein, BMP)修复牙种植体周围骨缺损的效果。方法: 60只兔子随机分成两组,在兔子的股骨预备种植窝后制造标准开放式骨缺损,宽3mm、高4mm、厚3mm,然后植入羟基磷灰石涂层的3. 3mm×8mmBLB种植体,一组骨缺损填入Bio-oss,另一组填入Bio-oss/BMP复合骨。于术后2、4和6个月取样本,制作带种植体的硬组织切片,进行组织学形态学观察,骨结合百分率测定和计算机组织图像定量分析。结果:两组的骨缺损处均有新骨形成,Bio-oss/BMP组与单独植入Bio-oss相比,新骨形成更早、新生骨量更多、骨的矿化程度更高。2、4和6个月的骨结合百分率均高于Bio-oss组。结论:Bio-oss是BMP理想的载体材料,Bio-oss/BMP复合骨可更快更有效的促进骨组织再生,并形成理想的种植体-骨结合界面。

毛细管电泳免疫化学发光检测鼠血管平滑肌细胞中zmol骨形成蛋白-2

In this study, a capillary electrophoresis immunoassay(CEIA) method based on the enhanced chemiluminescence(CL) detection was developed. A horseradish peroxidase(HRP) label catalyzing the luminol/H 2O 2/p-iodophenol(PIP) reaction was performed, and the HRP was detected with detection limit(S/N=3) of 4.4 pmol/L(53 zmol), which is one of the highest sensitivity of HRP reported yet. The HRP was linked to bone morphogenic protein-2(BMP-2) in rat vascular smooth muscle(VSM) cells in noncompetitive format and first detected by CL. HRP-Ab 2-mAb-BMP-2 complexes were baseline separated from free HRP label in 3 min. The detection limit(S/N=3) of BMP-2 is 6.2 pmol/L(75 zmol). This technique has been applied to arteriosclerosis pathology research. The change of BMP-2 contentin VSM cells which were stimulated by angiotensin Ⅱ(AgⅡ) for different hours was investigated in the concentration range of 1.0-10.0 pmol/L. The results are in accord with that obtained by common used Pathology image analysis system.

骨髓间质干细胞结合骨形态发生蛋白促进兔椎间关节融合的实验研究

[目的]探索应用骨髓间质干细胞结合骨形态发生蛋白进行脊柱前路融合的方法。[方法]自髂骨抽取骨髓4m,l在体外扩增出自体骨髓间质干细胞;对12只新西兰大白兔经前路腹膜外行腰椎间盘切除脊柱融合术。每只动物取3个脊柱节段随机接受4种移植方法:骨髓间质干细胞、骨形态发生蛋白和纤维蛋白胶(A组),骨髓间质干细胞和纤维蛋白胶(B组),骨形态发生蛋白和纤维蛋白胶(C组),纤维蛋白胶(D组)。实验动物在术后3个月处死,利用放射学和组织学方法观察、分析脊柱融合情况。[结果]A组的椎间隙骨痂形成明显较其他组多,组织学上有连续的骨痂形成;B组和C组显示出近似的放射学和组织学变化,有不连续骨痂生成。D组融合效果最差,为纤维肉芽组织填充椎间隙,无骨痂生成。[结论]自体骨髓基质干细胞、纤维蛋白和骨形态发生蛋白复合体在移植入体内3个月后有良好的成骨并初步获得椎体间融合。

骨形态蛋白-7对糖尿病大鼠nephrin表达和分布的影响

目的观察骨形态蛋白-7(BMP-7)对糖尿病(DM)大鼠nephrin表达和分布的影响。方法20只链脲左菌素(STZ)诱导的糖尿病大鼠模型随机分为糖尿病组(DM)和BMP-7治疗组(BMP-7)各10只,另以10只大鼠作对照组(NC)。BMP-7组每周2次腹腔注射人重组BMP-730μg/kg。DM组和NC组给予等量的生理盐水注射。于8、16、24周检测不同时间点24h尿蛋白、尿肌酐和血糖。24周处死动物,PAS染色和透射电镜观察肾组织学改变,RT-PCR、免疫荧光检测nephrin的表达和分布,免疫组化技术检测TGF-β1和WT1的表达。结果与NC组比,DM组24h尿蛋白、肾质量/体质量指数、TGF-β1的表达均显著高于NC组(F值分别为174.3、38.9、117.7,P均小于<0.01)差异均具有统计学意义。而内生肌酐清除率(Ccr)、足细胞数目、nephrin的表达显著低于NC组(F值分别为13.4、79.04、65.5,P均<0.01),而且nephrin由正常的沿毛细血管襻线状分布向颗粒状、团块状改变。BMP-7组24h尿蛋白、肾质量/体质量、TGF-β1的表达较DM组显著降低,Ccr、足细胞数目和nephrinmRNA的表达显著增加,且保持着正常的沿毛细血管襻线状分布,肾脏病理改变减轻。结论外源性的运用BMP-7可以有效地抑制糖尿病引起的nephrin表达的下调,维持nephrin在足细胞上的正常分布;BMP-7对糖尿病大鼠肾脏保护作用可能与拮抗了TGF-β1的活化有关。

兔自体骨髓基质细胞经皮移植修复骨缺损的实验研究

目的 :比较兔骨髓基质细胞 (MSC)与新鲜红骨髓经皮注射到骨缺损处后的成骨能力。方法 :1 8只新西兰兔经穿刺抽取骨髓培养 ,将扩增的MSC收集稀释成悬液 0 .5ml(细胞数约 5× 1 0 6) ,加入 1 0 0ngBMP后经皮注射到兔双侧桡骨缺损中的一侧 ( 1 8侧 ) ,对侧分别注射骨髓 0 .5ml (含BMP 1 0 0ng)( 1 3侧 )。分别于 2、 4、 8周行X线、组织病理学检查。结果 :X线、组织病理切片表明BMP +MSC组多数术后 2周有明显的骨痂生成 ,术后 4～ 8周形成骨性连接 ,新骨形成、骨改建及骨髓成熟度指标均优于对照组 ,两行差异有显著性意义 (P <0 .0 5 )。结论 :在相同条件下 ,体外扩增诱导的MSC较新鲜红骨髓有更强、更快的成骨能力。经皮注射MSCs +BMP能够迅速促进兔桡骨缺损处新骨形成 ,修复骨缺损。

VEGFmRNA与BMP-2在非创伤性股骨头坏死中表达的研究

[目的]探讨非创伤性股骨头发生坏死后局部的血管内皮生长因子(vascular endothelial growth factor VEGF)mRNA与骨形态发生蛋白-2(bone morphogenic proteins,BMP-2)表达的变化及其意义。[方法]收集经全髋置换术取下的非创伤性股骨头坏死的股骨头标本16例作为实验组,新鲜股骨颈骨折标本10例作为对照组。将股骨头自冠状面对半剖开,于坏死区、健存区各取1骨块,经固定、脱钙,制作切片,光镜、电镜观察其病理变化,并运用免疫组化及原位杂交技术分别对其BMP-2蛋白和VEGF mRNA表达情况进行检测。[结果]实验组组织结构紊乱,破碎,骨小梁稀疏、不完整,有大量的空骨陷窝,而对照组骨小梁相对较完整、排列整齐,骨小梁中的骨细胞清晰可见,核大,位于中央。实验组BMP-2蛋白和VEGF mRNA阳性表达的强度及面积均明显低于对照组,结果有统计学意义(P<0·05)。[结论]非创伤性股骨头坏死股骨头局部的BMP-2及VEGF mRNA表达降低,极有可能是导致其自身修复能力不足的重要原因。