大鼠角膜缘干细胞分离培养及其横向分化能力初探

目的体外分离培养大鼠角膜缘干细胞(LSCs),并探讨在细胞因子EGF、b FGF联合RA作用下,LSCs体外横向分化为神经干细胞样细胞的能力。方法体外分离培养LSCs并进行p63免疫组化鉴定。在原代培养的LSCs中,设立2个诱导组进行分化实验,诱导组1加入EGF(20 ng/mL)和b FGF(10 ng/mL),诱导组2加入EGF(20 ng/mL)、b FGF(10 ng/mL)和RA(25 ng/mL),同时设立空白对照组。培养7 d后,收集各组细胞作神经元标志物Nestin的免疫组化检测及阳性细胞计数,收集各组细胞蛋白做蛋白免疫印迹分析各组Nestin蛋白表达情况,相关数据作统计学分析。结果免疫组化结果显示,体外分离培养的LSCs p63呈阳性,诱导分化的2组细胞Nestin呈阳性表达,阳性率分别为(77.01±6.32)%和(84.01±5.43)%,诱导组2的诱导率高于诱导组1,差异具有统计学意义(P0.05);对照组细胞Nestin呈阴性表达。蛋白免疫印迹结果显示,2个诱导组在240 k Da处可见Nestin蛋白条带,诱导组2 Nestin蛋白表达略高于诱导组1,对照组未见Nestin蛋白条带。结论成功分离培养大鼠LSCs,在细胞因子EGF、b FGF作用下,LSCs具有横向分化为神经干细胞样细胞的能力,同时联合使用RA有促进LSCs向神经干细胞样细胞分化的作用。     

EGF和bFGF对成年大鼠神经干细胞增殖和分化的影响

本研究旨在探索可促进成年大鼠神经干细胞增殖并形成较多的克隆球以及其分化出较多神经元的因素。取成鼠前脑室下区的组织进行原代培养 ,将之分为三组分别加入 EGF、b FGF以及 EGF+ b FGF,观察克隆球的形成状况。一周后收集三组原代细胞克隆球 ,加入完全培养液 (仅含 10 %胎牛血清 )进行分化实验。分化 14 d后 ,分别用 MAP-2和 GFAP的单克隆抗体进行免疫荧光标记 ,计算阳性细胞数量。无血清培养结果显示 ,b FGF组和 EGF+ b FGF组原代培养液中形成的原代克隆球数量和直径的差别不明显 ,但都明显地大于 EGF组。免疫荧光结果显示 ,b FGF组和 EGF+ b FGF组中的克隆球分化出 MAP-2阳性神经元的数量明显多于 EGF组 ,而 EGF组则能产生较多的胶质细胞。提示 ,b F GF能促进成年大鼠神经干细胞增殖 ,所形成的细胞克隆球能分化为较多的神经元。     

小鼠胚胎干细胞来源的神经干细胞的稳定传代体系探索

目的探讨体外诱导、获取均一的神经干细胞群(NSCs)的有效方法,并建立神经干细胞体外稳定传代扩增体系。方法首先采用无血清的诱导培养基贴壁诱导mESCs形成神经上皮祖细胞(NPCs)。然后将经添加表皮生长因子(EGF)和成纤维细胞生长因子-2(FGF2)的无血清培养基短暂悬浮培养后的NPCs再贴壁培养,诱导形成NSCs。通过细胞系46C监测NPCs的形成,同时对分化细胞进行定量PCR和免疫荧光染色,在不同水平检测细胞分化效果。结果 mESCs神经诱导5 d出现大量Sox1+的NPCs;NPCs悬浮培养后,进一步诱导可得到形态均一的NSCs。第2代和第6代NSCs的神经干细胞标志定量PCR检测结果为:Pax6、Nestin、Mash1、BLBP高表达。第8代NSCs免疫荧光染色显示90%以上的细胞均为Nestin、RC2和Pax6阳性。结论成功诱导mESC生成神经干细胞群,并且可以在体外连续稳定的传代。     

丹参诱导骨髓基质细胞神经元样细胞分化的microRNA-128路径

目的　研究microRNA-128在丹参制剂诱导大鼠骨髓基质细胞(bone marrow strowal cells,BMSCs)向神经元样细胞分化过程中的调控作用。  方法　培养鉴定大鼠BMSCs,应用反义寡居核苷酸转染技术（Lipofectamin 2000）转染microRNA-128 inhibitors于BMSCs;取转染和未转染的BMSCs,待细胞增殖到60%~70%融合时进行预诱导分化,预诱导24 h后,进行诱导分化;根据处理方式不同分为4组：未诱导组（A组）,丹参制剂诱导组（B组）,转染未诱导组（C组）,转染诱导组（D组）。流式细胞术鉴定BMSCs;qPCR检测microRNA-128及神经元特异性烯醇化酶（NSE）、巢蛋白（Nestin）、微管蛋白（β3-tubulin）的mRNA表达;Western blot检测NSE、Nestin和β3-tubulin的蛋白表达。  结果    BMSCs流式细胞检测CD29和CD90双阳性率达99.17%,CD11b和CD45双阴性率达99.21%;丹参制剂诱导及microRNA-128 inhibitors转染后,细胞microRNA-128表达量显著降低（P<0.05）;诱导与未诱导组,转染与未转染组比较,NSE、Nestin和β3-tubulin的mRNA和蛋白表达均显著升高（P<0.05）。  结论　丹参制剂能够抑制BMSCs的microRNA-128表达,进而影响BMSCs神经分化相关蛋白的表达,促进BMSCs向神经元样细胞分化。     

bFGF和EGF诱导大鼠骨髓间充质干细胞分化成神经样细胞

 目的 探讨bFGF和EGF诱导大鼠BMSCs成神经分化潜能及其表型变化。方法 全骨髓贴壁法分离培养BMSCs,流式细胞仪检测P3代细胞表面标志物CD90、CD45。P3代细胞分为1）对照组（1%胎牛血清+DMEM/F-12）,2）EGF组(20ng/mLEGF）,3）bFGF组(20ng/mLbFGF),4）EGF+bFGF组(20ng/mLEGF+20ng/mLbFGF)行诱导,倒置相差显微镜观察细胞形态,Western blot检测细胞内NSE及GFAP蛋白的表达,RT-PCR检测其mRNA。结果 BMSCs呈长梭形或扁平形,漩涡样排列,CD90表达高达98.72%,而CD45仅1.05%;诱导后胞体收缩,折光性增强,呈双极甚至复杂的多极,向周围伸出明显突起,呈典型的神经样细胞;NSE、GFAP蛋白EGF组、bFGF组、EGF+bFGF组表达均高于对照组,bFGF组、EGF+bFGF组高于EGF组,且EGF+bFGF组高于bFGF组,EGF组高于对照组（p<0.05）;mRNA变化与上述结果类似。结论 bFGF和EGF可促进大鼠BMSCs向神经分化,二者合用时效果最显著,且bFGF促BMSCs向神经分化的能力强于EGF。为BMSCs移植治疗周围神经疾患提供了理论基础。     

GM1联合生长因子诱导骨髓间充质干细胞分化为神经元样细胞的研究

目的:探讨单唾液酸四己糖神经节苷脂(monosialoteterahexosyl ganglioside,GM1)联合生长因子(bFGF+EGF)能否更为高效地促进骨髓间充质干细胞(bone marrow mesenchymal stem cells,BMSCs)分化为神经元样细胞,从而为细胞替代治疗缺血性脑卒中提供实验依据。方法:采用密度梯度离心法获取骨髓单个核细胞,行原代、传代培养,取第3代BMSCs,用流式细胞术鉴定其表面标志物;同时鉴定其多分化潜能。将第3代BMSCs分四组向神经元样细胞诱导分化,A组:单用(bFGF+EGF);B组:单用GM1;C组:GM1联合(bFGF+EGF);D组:对照组。分别在正式诱导前后行免疫细胞化学法检测各组细胞Nestin、β-TubulinⅢ、GFAP的阳性表达率并行数据统计分析。结果:流式细胞术鉴定BMSCs表面标志物呈CD29(+)、CD105(+)、CD34(-)、CD45(-);同时其具分化为成骨细胞和成脂细胞潜能。BMSCs诱导为神经元样细胞之前,四组细胞Nestin、β-Tubulin、GFAP表达均呈阴性;诱导2~4 d时,A、B、C三组Nestin阳性细胞表达率均呈上升趋势,且C组高于A、B、D组;诱导6~8 d时,A、B、C三组Nestin阳性细胞表达率均有所降低,而β-TubulinⅢ、GFAP阳性细胞表达率则呈较明显上升趋势,且C组较A、B组升高明显。综合实验数据,C组Nestin、β-TubulinⅢ、GFAP阳性细胞表达率均高于A、B、D组。结论:GM1联合生长因子(bFGF+EGF)相比单独的生长因子(bFGF+EGF)或GM1,可更为高效地促进BMSCs诱导分化为神经元样细胞。     

联合应用EGF和NGF对成年大鼠海马神经干细胞分化的影响

目的探讨联合应用表皮生长因子(EGF)和神经生长因子(NGF)对成年大鼠海马神经干细胞(NSCs)分化的影响。方法用含碱性成纤维生长因子(bFGF)、表皮生长因子、B27的无血清细胞培养技术体外培养成年大鼠海马神经干细胞,单克隆培养细胞行Nestin免疫细胞化学染色,诱导分化1w后细胞行GFAP和NSE免疫细胞化学染色;根据培养基中所加营养因子的不同将第4代细胞分为4组培养:EGF组、EGF+NGF组、NGF组、对照组,此4组细胞培养1w后行NSE免疫细胞化学染色,计数阳性细胞比例后进行统计学分析。结果单克隆培养后克隆球表达Nestin,诱导分化1w后细胞表达NSE、GFAP。与空白对照组相比,EGF组、NGF组和EGF+NGF组细胞分化为神经元的比例较高(P<0.05),其中EGF+NGF组细胞的比例最高。结论单独或联合应用EGF、NGF可以促进成年大鼠海马神经干细胞向神经元分化。     

BMSCs移植通过T细胞免疫抑制缓解1型糖尿病小鼠发病实验研究

目的　探讨小鼠骨髓间充质干细胞（Bone marrow mesenchymal stem cells, BMSCs）移植缓解1型糖尿病小鼠（T1DM）发病及机制。 方法　BMSCs分离培养及鉴定;第3代培养的上清作为条件培养基,与2周龄NOD小鼠脾细胞共培养,FACS检测CD4+和CD8+T细胞增殖及活化;2周龄雌性NOD小鼠随机分为BMSCs组、PBS组、对照组,每组6只,对照组2周处死;BMSCs组和PBS组12周分别腹腔注射100 μl（2×107细胞）BMSCs或等体积PBS,监测小鼠血糖和体重至26周;HE、免疫组化、免疫荧光染色观察胰腺炎性细胞浸润;FACS检测CD4+和CD8+T细胞增殖及活化。 结果　成功分离培养BMSCs;BMSCs条件培养基抑制CD4+及CD8+T细胞的增殖及活化（P<0.05）;BMSCs组小鼠体重高于PBS组（P<0.05）,糖尿病发病率降低,炎性浸润减少（P<0.05）,脾脏CD4+和CD8+T细胞增殖及活化降低（P<0.05）。结论　BMSCs移植可能通过T细胞免疫抑制缓解T1DM小鼠发病。     

BMSCs移植通过T细胞免疫抑制缓解1型糖尿病小鼠发病实验研究

目的　探讨小鼠骨髓间充质干细胞（Bone marrow mesenchymal stem cells, BMSCs）移植缓解1型糖尿病小鼠（T1DM）发病及机制。 方法　BMSCs分离培养及鉴定;第3代培养的上清作为条件培养基,与2周龄NOD小鼠脾细胞共培养,FACS检测CD4+和CD8+T细胞增殖及活化;2周龄雌性NOD小鼠随机分为BMSCs组、PBS组、对照组,每组6只,对照组2周处死;BMSCs组和PBS组12周分别腹腔注射100 μl（2×107细胞）BMSCs或等体积PBS,监测小鼠血糖和体重至26周;HE、免疫组化、免疫荧光染色观察胰腺炎性细胞浸润;FACS检测CD4+和CD8+T细胞增殖及活化。 结果　成功分离培养BMSCs;BMSCs条件培养基抑制CD4+及CD8+T细胞的增殖及活化（P<0.05）;BMSCs组小鼠体重高于PBS组（P<0.05）,糖尿病发病率降低,炎性浸润减少（P<0.05）,脾脏CD4+和CD8+T细胞增殖及活化降低（P<0.05）。结论　BMSCs移植可能通过T细胞免疫抑制缓解T1DM小鼠发病。     

重组γ-神经胶质成熟因子诱导体外神经干细胞分化为星形胶质细胞

目的探索γ-神经胶质成熟因子(GMFG)能否促进大鼠神经干细胞增殖并分化成神经胶质细胞。方法无菌分离大鼠胚胎脑组织进行原代培养和传代培养,将第3代含有神经球的培养基制成细胞悬液,经Nestin免疫荧光染色检测呈阳性后,分4组培养,1组、2组每天分别加入5μg/L、10μg/L重组GMFG,3组加入10%胎牛血清(FBS),对照组为培养基。结果对照组细胞培养4 d后见少数细胞增殖并长出细长的分支;FBS组细胞培养3 d后大量增殖并分化,形态学上为原浆型星形胶质细胞,呈扁平片状贴在培养皿表面;GMFG组细胞培养2 d后大量增殖并分化,形态学上为纤维型星形胶质细胞,5μg/L组细胞分化不如10μg/L组细胞分化明显。结论GMFG能诱导神经干细胞在体外增殖并分化为星形胶质细胞。     

脊髓缺血再灌注损伤对大鼠水通道蛋白4表达的影响

目的:在整体水平研究脊髓缺血再灌注损伤对大鼠水通道蛋白4表达水平的影响.方法:SD大鼠72只随机分为空白组、假手术组和SCⅡ组,每组24只.建立大鼠脊髓缺血再灌注损伤模型,并于1、3、5、7天四个时间点分别处死6只.BBB评分评价神经功能,Western blot和免疫荧光方法检测AQP4的表达情况.结果:空白对照组和假手术组在不同时间点的BBB评分均为21分,SCⅡ组的BBB评分在1天时最低,随时间推移逐渐增加,3天明显优于1天(P＜0.05),5天明显优于3天(P＜0.05),5天明显优于7天(P＜0.05).Western blot在34 kD及43 kD分子量处可见特异性条带,SCⅡ组早期AQP4的表达水平显著下降,即在1、3、5、7天四个时间点AQP4的表达显著低于空白对照组和假手术组,但呈逐渐增加趋势;在7天仍显著低于正常空白组和假手术组(P＜0.05).免疫荧光检测AQP4的表达变化趋势与Western blot的检测结果相似.结论:SCⅡ存在AQP4低表达,这可能是造成SCⅡ神经功能障碍的重要原因.     

Inhibition of very late antigen-4 and leukocyte function-associated antigen-1 in experimental autoimmune uveoretinitis

B10.RIII mice were immunized with interphotoreceptor retinoid binding protein peptide to induce uveitis. Mice were injected intraperitoneally with anti-very late antigen-4 (VLA-4), anti-leukocyte function-associated antigen-1 (LFA-1), or a control Ab every other day from Day 5 to Day 13 post-immunization. The eyes and spleens were harvested on Day 14 or 28. The eyes were used for histologic/cytokine mRNA expression analyses. The spleens were used for Ag-recall cytokine production assays and intracellular cytokine assays. Treatment with both Abs led to a profoundly significant reduction in severity of uveitis and cytokine mRNA expression in the eye. However, cytokine production by splenocytes was significantly upregulated. Discontinuation of Ab treatment led to an increase in uveitis severity and cytokine mRNA expression in the eye, but led to a decrease in cytokine production and intracellular IFN-γ⁺ and IL-17A⁺cytokine profile by splenocytes. Thus, blockade of these molecules using specific Abs may be a therapeutic option for patients with uveitis; however, such treatment must be continued.     

Roles of Toll-Like Receptor 4 for Cellular Pathogenesis in Primary Open-Angle Glaucoma: A potential therapeutic strategy

In recent years, glaucoma has been proposed as an autoimmune disease and an understanding immune-regulation concept has been applied for novel glaucoma therapy. Current evidence suggests an innate immunity is a keystone step for primary open angle glaucoma (POAG) pathogenesis resulting from trabecular meshwork (TM) cell fibrosis and retinal ganglion cell (RGC) death. Toll-like receptor 4 (TLR4) is a common player in the innate immunity, which appears on the TM and RGC of POAG. The activation of TLR4 regulates several molecules involving both fibrosis and cell death. Inhibition of TLR4 decreases TGF-β2-induced fibrosis in TM cells and enhances cell survival of RGC in both optic nerve crush and ischemia models. In this review, we will summarize the molecular mechanisms of TLR4 related to POAG pathogenesis. An understanding of this mechanism may provide novel development of therapeutic strategies for POAG.     

Transgenic overexpression of anti-double-stranded DNA autoantibody and activation of Toll-like receptor 4 in mice induce severe systemic lupus erythematosus syndromes

Systemic lupus erythematosus (SLE) is a multi-organ autoimmune disease characteristized by the presence of autoantibodies against double-stranded DNA (anti-dsDNA) in sera at high levels. Bacterial infections in SLE are associated with higher morbidity and mortality. Our goal was to observe the interaction between these 2 factors in the pathogenesis of lupus. We generated transgenic mice with monoclonal anti-dsDNA to investigate the development of lupus. By challenging the mice in vitro and in vivo with Toll-like receptor 4 (TLR4) ligand lipopolysaccharides (LPS), we were able to examine the role of bacterial infection in SLE. In our study, the transgenic mice with a secreted form of anti-dsDNA were found to have higher levels of anti-nuclear antibodies, anti-dsDNA, blood urea nitrogen, and proteinuria. The splenocytes of the mice stimulated with LPS secreted more anti-dsDNA, IFN-γ, and IL-10. After injecting them with LPS in vivo, we further found higher immune complex depositions and IL-10 in the kidneys of the transgenic mice. Moreover, the LPS-injected transgenic mice had higher mortality rate. This is the first transgenic model to demonstrate that only 2 risk factors, pathogenic anti-dsDNA and TLR4 activation, induce severe SLE syndromes in normal mice through the overproduction of IL-10 and IFN-γ. These findings imply that anti-dsDNA and bacterial infections have pivotal roles in the pathogenesis of SLE; the inhibition of TLR4 may be regarded as a therapeutic target.     

卵巢癌患者血清Hcy、HFA和SA联检的临床意义

目的：探讨了卵巢癌患者血清Hcy、HE4和sA联检的变化及临床意义。方法：应用酶联法和生化法对33例卵巢癌患者进行了血清Hcy、HFA和sA的检测,并与35例正常健康人作比较。结果：卵巢癌患者血清Hcy、HE4和SA水平均非常显著地高于正常人组（P〈0．01）。且血清Hcy水平与HE4、SA水平呈正相关（r=0．6128、0．5942,P〈0．01）。结论：检测卵巢癌患者血清Hcy、HFA和SA水平的变化,提示该类生物标志物的变化,有助于对疾病早期诊断和适宜的预后。     

The regulation effect of ulinastatin on the expression of SSAT2 and AQP4 in myocardial tissue of rats after cardiopulmonary resuscitation

Objective: This study aims to investigate the regulation effects of ulinastatin (UT1) on the expression of spermidine/spermine -N1-acetyltransferase 2 (SSAT2) and aquaporin 4 (AQP4) in myocardial tissue of rats after cardiopulmonary resuscitation (CPR) and their correlations. Methods: A total of 90 adult SD rats were divided into sham operation group (A, n=30), model group (B, n=30) and UT1 group (C, n=30). The cardiac arrest (CA) and CPR model was established by asphyxia method. Left ventricular fractional shortening (LVFS), left ventricular ejection fraction (LVEF) and E/A peak ratio of mitral valve in three groups were collected by ultrasonic echocardiography. Apoptosis of myocardial cells was detected by DAPI staining. The expression levels of SSAT2 and AQP4 were detected by RT-PCR, Western blotting and immunohistochemical methods. Results: UT1 could significantly improve the levels of LVFS, LVEF and E/A ratio and decrease myocardial cell apoptosis. As compared with group B, the expression level of SSAT2 increased and the expression level of AQP4 decreased in group C (P<0.01). SSAT2 was the most in group A and the least in group B while AQP4 was the least in group A and the most in group B (P<0.01). There was positive correlation between SSAT2 and cardiac function in CRP model while there was negative correlation between AQP4 and cardiac function (P<0.01). The expression of SSAT2 and AQP4 protein in myocardial tissue was negatively correlated in CRP model (r=-0.920, P<0.01). Conclusions: UT1 can effectively reduce the cardiac function damage caused by CRP, which could be related with the increased SSAT2 and decreased AQP4.     

自身免疫性甲状腺病CTLA—4基因外显子1A／G^49多态性研究

目的　探讨细胞毒性T淋巴细胞相关抗原4（CTLA-4）基因外显子1的49位点A／G多态性与自身免疫性甲状腺病（AITDs）的相关性。方法　采用多聚酶链反应限制性片段长度多态性（PCR-RFLP）技术分析122例自身免疫甲状腺病患者,其中Graves’病（GD）87例,桥本甲状腺炎（HT）35例,84例健康对照的CTLA-4基因外显子1的49位点基因型。采用ELISA技术检测AITDs患者甲状腺功能,间接免疫荧光法检测甲状腺球蛋白抗体（TGAb）和甲状腺抗过氧化物酶抗体（TPOAb）。结果　AITDs患者CTLA-4／G     

Gene Polymorphism of Interleukin-4, Interleukin-4 Receptor and STAT6 in Children with Atopic Dermatitis in Taif,Saudi Arabia

Aim of study: This work was performed to evaluate the level of IL-4, and to clarify the role of IL-4 gene polymorphism at position cytosine –590-to-thyamine (C-590T), IL-4Rα gene polymorphism at position adenine +4679-to-guanine (A+4679G) [isoleucine-50-valine (I50V)] and STAT6 gene polymorphism at position guanine 2964-to-adenine (G2964A) in Saudi children with non-atopic dermatitis (non-AD) and atopic dermatitis (AD) to identify their role in the pathogenesis of these diseases.

Subjects and methods: This study included 150 children: 50 healthy children as controls, 50 with non-AD, and 50 with AD. They were subjected to full clinical examination, complete blood picture, skin prick test, and determination of serum interleukin-4 (IL-4) and total immunoglobulin-E (IgE) levels. Detection of interleukin-4 gene (C-590T), interleukin-4 receptor alpha gene (A+4679G) (I50V), and STAT6 gene (G2964A) polymorphisms were performed by PCR-based restriction fragment length polymorphism (PCR-RFLP).

Results: There was a significant (P < 0.01) association between genotype and allele frequencies of IL-4Rα (A+4679G) (I50V) polymorphism in the AD group (but not non-AD group). Moreover, there was a significant association between genotype and allele frequencies of the STAT6 (G2946A) polymorphism in the non-AD (P < 0.05) and AD (P < 0.01) groups. On the other hand, there was no significant association between genotype and allele frequencies of the (C-590T) polymorphism in the non-AD group and AD group. There was a significant (P < 0.001) higher total IgE level in patients compared to the controls. Moreover, the mean values of total IgE were significantly different among the different allelic variants of (C-590T), (I50V), (G2964A) polymorphisms of IL-4, IL-4Rα, and STAT6 genes, respectively, in all the studied groups. On the other hand, there was no significant difference of serum IL-4 levels among all the studied patients, or among the different allelic variants of (C-590T), (I50V), (G2964A) polymorphisms of IL-4, IL-4Rα, and STAT6 genes, respectively.

Conclusion: IL-4Rα gene (I50V) and STAT6 gene (G2964) polymorphisms may play a role in development of eczema; however, the IL-4 gene polymorphism (C-590T) had no relationship with susceptibility to the disease among Saudi children.     

卵巢癌患者血清HE4、CA125和血浆LPA水平变化及其临床意义

目的:探讨血清HE4、CA125和血浆LPA水平在卵巢癌患者中的变化及其临床意义.方法:分别应用单克隆夹心ELISA、放射免疫分析和化学法定量检测50例卵巢癌患者血清HE4、CA125和血浆LPA含量,并与正常对照组比较分析.结果:卵巢癌Ⅲ/Ⅳ期患者血清CA125和血浆LPA水平均显著高于Ⅰ/Ⅱ期(P<0.01),而血...     

睾丸孤核受体4（TR4）促进巨噬细胞向前列腺癌浸润

目的：研究前列腺癌TR4水平对巨噬细胞浸润的影响。方法：用transwell体系进行巨噬细胞THP-1迁移实验,在人体组织中研究睾丸孤核受体4(Testicular orphan receptor 4,TR4)水平和巨噬细胞标志物CD36的关系。结果：过表达TR4促进了巨噬细胞向前列腺的迁移;敲低TR4抑制了巨噬细胞向前列腺癌的迁移;人体前列腺癌组织标本中TR4较高的患者,CD36表达较高。结论：前列腺癌的TR4可能促进了巨噬细胞浸润。