肝癌组织中人宫颈癌癌基因mRNA的表达及意义

目的 观察人宫颈癌癌基因(HCCR)mRNA在肝癌和癌旁正常组织以及肝癌患者和正常人外周血单个核细胞(PBMC)中的表达水平.方法 TRIZOL法提取肝癌组织和癌旁正常肝组织以及肝癌患者和正常人的PBMC的RNA,用RT-PCR技术分析HCCR基因在不同样品中的mRNA表达水平.结果 在肝癌组织中,HCCR的mRNA相对表达强度为0.776±0.101,癌旁正常组织中的相对表达强度0.470±0.154,两者相比,P＜0.05.在PBMC中,肝癌患者HCCR mRNA的表达强度为0.256±0.069,而正常人未检测出,两者相比,P＜0.05. 结论 HCCR基因可能参与了肝癌的发生与发展,与肝癌的病理过程有一定的相关性.     

神经生长因子在原发性肝癌中的表达及其临床意义

目的 观察神经生长因子(NGF)在原发性肝癌组织中的表达及在患者血清中的含量,了解血清NGF水平与肝癌临床病理特征的关系. 方法 26例肝细胞癌及对应癌旁组织,采用半定量PCR、免疫印迹及免疫组织化学分析NGF mRNA和蛋白的表达及其分布.健康对照者、慢性肝炎、肝硬化及肝癌患者共150例,采用酶联免疫吸附法(ELISA)检测血清NGF的水平,分析其临床意义.两组之间差异的显著性比较用t检验、Mann-Whitney U检验,多组之间差异的显著性比较应用Kruskal-Wallis H检验.数据均采用SPSS 11.5统计软件处理.结果 肝癌组织中NGF在mRNA及蛋白水平的表达高于癌旁组织,NGF主要分布于肝细胞胞质.血清NGF水平:肝癌组、肝硬化组、慢性肝炎组患者和正常对照组分别为(33.86±16.11)pg/ml、(20.57±9.73)pg/ml、(13.20±6.23)pg/ml和(11.13±6.12)pg/ml,肝癌组、肝硬化组显著高于慢性肝炎组患者和正常对照组,x2值分别为39.119和12.041,P值均＜0.01.肿瘤直径大于5cm及TNM分级为Ⅲ、Ⅳ级的肝癌患者血清NGF的水平高于肿瘤直径小于5cm及TNM分级为Ⅰ、Ⅱ级的患者.结论 NGF在肝癌组织中高表达,肝癌患者血清NGF水平明显升高,与肿瘤体积和TNM分级相关,提示NGF在肝癌的发生和发展过程中可能发挥一定作用,血清NGF有助于肝癌患者的病情评估和预后估计.     

内皮细胞特异性因子ESM-1在肝癌血管内皮细胞的表达及作用

目的本研究拟通过分离纯化肝癌的血管内皮细胞，检测内皮细胞特异性分子1（ESM-1）在肝癌内皮细胞中的表达，并探讨其变化与肿瘤血管生成和侵袭的关系。方法收集山东大学附属省立医院肝胆外科行手术切除治疗且经术后病理证实的新鲜肝癌组织和癌旁组织。应用CD31单抗标记的免疫磁珠法进行分离并纯化血管内皮细胞，经内皮细胞鉴定并分析细胞纯度，应用荧光实时定量PCR、Westernblot等方法检测血管内皮细胞中ESM-1的表达。应用酶联接免疫吸附剂测定（ELISA）法检测相应肝癌患者及正常对照者血清中ESM-1的水平。结果经测定，ESM-1在肝癌患者血清中为（12．643±2．280）ng／mL，相比正常对照（4．660±1．172）ng／mL表达水平明显升高（t=10．16，P〈0．01），同时，在肝癌内皮细胞中ESM-1的mRNA和蛋白水平的表达均明显升高。结论ESM．1可能参与了肝癌的血管生成和侵袭过程，有望作为新的肿瘤治疗靶点。     

mTOR/P70S6K信号通路在肝细胞肝癌中的表达及临床意义

目的:研究mTOR/P70S6K信号通路在肝细胞肝癌(HCC)中的表达,探讨其在HCC发生发展中的作用及意义.方法:用逆转录聚合酶链反应(RT-PCR)技术检测120例HCC患者癌组织、癌旁肝组织以及10例正常肝组织中mTOR及P70S6K mRNA表达情况;并分析mTOR及P70S6K mRNA的表达与相关临床参数的关系.结果:mTOR及P70S6K mRNA在HCC组织中的表达水平显著高于在癌旁肝组织和正常肝组织中的表达水平(mTOR mRNA:0.594±0.218 vs 0.437±0.156.0.594±0.218 vs 0.383±0.081,均P＜0.05;P70S6K mRNA:0.610±0.147 vs 0.486±0.162.0.610±0.147 vs 0.440±0.141,均P＜0.05).mTOR mRNA和P70S6KmRNA在HCC组织中的表达呈正相关(r=0.548,P=0.012),且两者在癌旁肝组织及正常肝组织中的表达亦正相关性(r=0.607,0.737,P=0.005,0.015).mTOR及P70S6K mRNA在HCC组织中的表达水平与病理分期、门静脉癌栓等明显相关,而与肿瘤直径、血清AFP水平、性别等无明显关系.结论:mTOR/P70S6K信号通路在HCC中特异性激活.mTOR/P70S6K信号通路可能在肝细胞肝癌的发生、发展中起重要作用.     

肝癌患者可溶性肿瘤坏死因子受体Ⅱ检测的临床意义

目的 进一步了解肝癌患者的异常免疫状态,探讨血清、腹水sTNFRⅡ检测的临床意义.方法 用双单抗夹心酶免疫吸附法检测25例肝癌、25例肝硬化患者血清腹水中和30例正常人血清sTNFR Ⅱ水平.结果 肝癌病人血清sTNFR Ⅱ浓度[(9.39±4.10)ng/ml]显著高于正常人和肝硬化患者(P＜0.01),同时肝硬化患者血清sTNFR Ⅱ浓度[(0.58±0.18)ng/ml]明显高于正常人[(0.31±0.16)ng/ml,P＜0.01].肝癌病人腹水sTNFRⅡ浓度[(9.13±5.26)ng/ml]亦显著高于肝硬化腹水sTNFR Ⅱ水平[(0.52±0.15)ng/ml,P＜0.01].肝癌、肝硬化患者血清、腹水sTNFR Ⅱ水平显著相关(r=1.00,P=0.00).肝癌血清sTNFRⅡ水平与外周血AFP和血小板数量呈正相关(r=0.432,P=0.05和r=0.513,P=0.03).结论 sTNFRⅡ的检测对反映肝癌患者的异常免疫状态,对肿瘤诊断具有实用价值.     

B细胞激活因子和增殖诱导配体与原发性干燥综合征发病机制的研究

目的 探讨原发性干燥综合征(pSS)患者B细胞激活因子(BAFF)和增殖诱导配体(APRIL)的表达情况及其与发病机制的关系.方法 分别采用酶联免疫吸附试验(ELISA)法、实时荧光定量反转录聚合酶链反应(RT-PCR)法、免疫组织化学方法检测pSS患者血清、外周血单个核细胞(PBMC)、唇腺组织中BAFF、APRIL的表达情况,分析其相互关系及与临床指标相关性.结果 pSS患者的血清BAFF高于健康对照组[(7.4±3.9)ng/ml和(3.7±1.1)ng/ml,P＜0.01]、血清APRIL高于健康对照组[(26±15)ng/ml和(16±15)ng/ml,P=0.039];且血清BAFF与IgG浓度、红细胞沉降率(ESR)、总球蛋白水平、抗核抗体(ANA)滴度相关(r＝0.490,0.402,0.429,0.406,P＜0.05),血清APRIL与ESR、唇腺淋巴细胞灶数相关(P＜0.05),两者均与外周血白细胞、血小板计数呈负相关(r=0.046.0.541,P＜0.05).pSS患者唇腺组织BAFF和APRIL蛋白表达在淋巴细胞浸润区均高于对照组(P＜0.05).而PBMC的BAFF mRNA表达相对量低于对照组[(0.023±0.024)和(0.245±0.188),P＜0.01],APRIL mRNA表达相对量均低于对照组[(0.047±0.035)和(0.130±0.097),P=0.002].血清BAFF与APRIL水平呈正相关(r＝0.534,P=0.002).结论 pSS患者BAFF和APRIL在血清、唇腺组织淋巴细胞浸润区表达异常增高并与临床指标相关,提示该系统可能参与pSS的发病过程;PBMC的BAFF、APRIL mRNA表达相对量的降低提示血清BAFF、APRIL蛋白的分泌产生和调节可能存在更复杂的机制.     

涎腺腺样囊性癌组织中ESM-1 mRNA及其蛋白表达的关系

目的探讨内皮细胞特异性分子-1（ESM-1）mRNA及其蛋白在涎腺腺样囊性癌组织中的表达及意义。方法采用地高辛标记eDNA探针原位杂交方法、免疫组织化学法,检测52例涎腺腺样囊性癌及11例癌旁正常涎腺组织中ESM-1 mRNA及其蛋白的表达。结果涎腺腺样囊性癌的ESM-1 mRNA及其蛋白高表达率显著高于癌旁正常涎腺组织（P〈0．01）,与患者性别、肿瘤组织学类型、有无淋巴结转移及侵犯神经无明显差异。涎腺腺样囊性癌组织和正常涎腺组织中ESM-1 mRNA和蛋白表达具有相关性。结论ESM-1分子与涎腺腺样囊性癌的发生可能有关。     

Visfatin在妊娠糖尿病孕妇血清及胎盘组织中的表达

目的 通过测定妊娠糖尿病(GDM)及正常妊娠妇女血清visfatin、胎盘组织visfatin及过氧化物酶体增殖物活化受体(PPAR)γ的表达,探讨visfatin、PPARγ在GDM中的作用及相互关系.方法 选取2011年10月至2012年10月在河北省人民医院妇产科行择期剖宫产终止妊娠的患者57例,其中GDM组30例、正常妊娠组27名.酶联免疫吸附法测定血清visfatin水平,实时荧光定量反转录PCR测定胎盘组织visfatin及PPARγ mRNA表达水平,免疫蛋白印迹法检测胎盘组织visfatin及PPARγ蛋白的表达水平.结果 GDM组产前血清visfatin水平明显低于正常妊娠组[(6.72±3.79)ng/ml vs.(8.87±4.08) ng/ml,t=-2.06,P=0.04];胎盘组织visfatin mRNA及蛋白表达水平在两组间无明显差异(P＞0.05);GDM组PPARγ mRNA及蛋白表达水平低于正常妊娠组[(0.26±0.11)vs.(0.60±0.41),t=-2.77,P＜0.05;(0.34 ±0.09)vs.(0.73±0.13),t=-7.03,P＜0.05],在GDM组,胎盘组织visfatin mRNA表达与PPARγ mRNA表达水平呈正相关(r=0.67,P=0.02).结论 Visfatin在GDM的发病中起一定作用,并与胎盘组织中PPARγ mRNA表达相关.     

肝癌组织中TGF-β1、TGF-β1RⅡ和NF-κB的表达

目的:探讨转化生长因子β1(TGF-β1)、转化生长因子β1Ⅱ型受体(TGF-β1RⅡ)、核转录因子-κB(NF-κB)在肝细胞癌(HCC)中表达.方法:在30例肝癌组织和癌旁肝组织中,用免疫组化技术,分别检测TGF-β1 TGF-β1RⅡ及NF-κB蛋白的表达;用原位杂交方法检测TGF-β1mRNA的表达,以CD34标记血管内皮细胞,观察TGF-β1及TGF-β1RⅡ蛋白与微血管密度(MVD)、TGF-β1蛋白与TGF-β1mRNA、NF-κB与TGF-β1的关系.结果:肝癌组织TGF-β1mRNA平均光密度明显高于癌旁组织(0.1 043±0.035 vs 0.0 620±0.0 225,P＜0.01)、TGF-β1蛋白平均光密度表达明显高于癌旁组织(0.0 72 5±0.0 102 vs 0.0 442±0.0 103,P＜0.01);肝癌组织TGF-β1RⅡ蛋白平均光密度表达明显低于癌旁组织(0.0 402±0.0 113 vs 0.0 669±0.0 157,P＜0.01);肝癌组织NF-KB蛋白表达均明显高于癌旁组织(0.0 723±0.0 210 vs 0.0 305±0.0116,P＜0.01),肝癌组织MVD明显高于癌旁组织(31.23±9.25 vs 4.24±2.10,P＜0.01),肝癌组织TGF-β1蛋白阳性表达与MVD呈正相关(t=3.25,P＜0.01);TGF-β1 mRNA与TGF-β1蛋白呈正相关(χ2=8.21,P＜0.01);NF-κB蛋白阳性表达与TGF-β1蛋白阳性表达呈正相关(χ2=9.075,P＜0.01);而TGF-βRⅡ蛋白与MVD呈负相关.结论:肝癌组织中TGF-β1基因的变化发生在多个水平,肝癌细胞中TGF-β1RⅡ、NF-KB蛋白表达异常,并与MVD相关,提示他们在肝细胞癌血管形成中发挥重要作用,NF-κB可能在介导TGF-β1的活化或产生中发挥一定的作用.     

肝癌组织巨噬细胞移动抑制因子的表达及对肿瘤细胞增殖和血管形成的影响

目的:研究巨噬细胞移动抑制因子(MIF)在原发性肝癌中的表达及对肝癌细胞增殖和血管形成的影响.方法:免疫组化法检测40例肝癌、癌旁组织和10例正常肝组织中MVD及MIF,IL-8和VEGF蛋白的表达情况,RQ-PCR检测MIF,IL-8和VEGF的mRNA表达水平.MTT法检测人重组MIF(rMIF)对Bel-7402肝癌细胞株增殖的影响,酶联免疫吸附试验(ELISA)和实时定量聚合酶链反应(RQ-PCR)检测VEGF和IL-8的分泌和mRNA的表达.结果:MIF,VEGF和IL-8在肝癌组织中均高表达(72.5%,67.5%,62.5%),经χ2检验,与正常组织相比(30.0%,20.0%,30.0%),差异具有显著性(P＜0.01).MIF和IL-8的表达与VEGF的表达呈正相关(r=0.271,P＜0.05),并且与MVD显著相关(r=0.284,P＜0.05).rMIF和Bel-7402共培养24 h后,上清中VEGF含量为900±265 ng/L,对照组为180±50 ng/L(P＜0.01),而IL-8含量改变无明显的变化(P＞0.05);实验组肝癌细胞株VEGF mRNA表达量是对照组的6.86倍(P＜0.05);而IL-8 mRNA是对照组的1.23倍(P＞0.05).结论:MIF是一种血管生成因子,MIF和IL-8的参与肿瘤血管形成有可能是通过VEGF发挥作用.     

Characterization of the secreted form of endothelial-cell-specific molecule 1 by specific monoclonal antibodies

Endothelial-cell-specific molecule 1 (ESM-1) is a recently identified endothelial cell molecule. As ESM-1 mRNA is preferentially expressed in human lung and kidney tissues, and as ESM-1 mRNA expression is regulated by inflammatory cytokines, ESM-1 is thought to play a role in the vascular contribution to organ-specific inflammation. In order to define its behavior, mouse anti-ESM-1 monoclonal antibodies were developed, and three distinct epitopes were mapped, which allowed development of a specific ELISA assay, immunohistological staining and immunoblot analysis. Here, we demonstrate that ESM-1 is present in cell lysates of human endothelial cells (human umbilical vein endothelial cells) with an apparent molecular weight of 20 kD. In contrast, the secreted form of ESM-1 is shifted to an apparent molecular weight of 50 kD, indicating that the secreted form of ESM-1 is posttranslationally modified. By ELISA, we show that the secretion of ESM-1 is significantly enhanced in the presence of TNFalpha. In contrast, the spontaneous as well as TNFalpha-induced secretion of ESM-1 is strongly inhibited by IFNgamma. Moreover, ESM-1 was detected in the serum of healthy subjects at an average concentration of 1.08 ng/ml, and we demonstrated that the serum level of ESM-1 is dramatically increased in patients presenting a septic shock. Analysis of ESM-1 expression in normal human tissues by immunohistochemistry showed that ESM-1 is localized in the vascular network, but also in the bronchial and renal epithelia. Our results demonstrate that ESM-1 is mainly expressed in the vascular endothelium both in vitro and in vivo, but also by different epithelia. ESM-1 may represent a new marker of endothelial cell activation, and may have a functional role in endothelium-dependent pathological disorders.     

胰腺癌HMGB1表达及其与血行转移的关系研究

目的 探讨人胰腺癌高迁移率族蛋白B1(hiish mobility group protein B1,HMGB1)表达及其与血行转移的关系.方法 应用Western blot法检测68例胰腺癌患者、18例CP和21例健康者血清HMGB1水平,并对其中37例胰腺癌患者手术前后的血清HMGB1水平进行比较;应用免疫组织化学法检测67例胰腺癌组织HMGB1和CD31的表达.结果 胰腺癌、CP及健康者血清HMGB1水平分别为(119.7±54.5)ng/ml、(40.2±25.5)ng/ml和(13.1±4.3)ng/ml,相差非常显著(P<0.001).胰腺癌患者术后血清HMGB1水平为(69.3±5.1)ng/ml,显著低于术前的(120.2±8.2)ng/ml(P<0.001).胰腺癌组织HMGB1表达阳性率为43.6%,HMGB1表达与组织分化、TNM分期及转移有关,P均<0.01;HMGB1表达与血管密度呈显著正相关(r=0.76,P<0.0001),免疫组化显示,HMGB1表达阳性的肿瘤细胞多位于有腔血管周围,位于血管内的肿瘤细胞HMGB1阳性表达率为71%.结论 胰腺癌患者HMGB1呈高表达,表达HMGB1的肿瘤细胞易于进入血管内,与其血行转移有关.     

胰腺内分泌肿瘤ghrelin和受体GHS-R1A的表达及患者血浆ghrelin、瘦素水平

目的 检测胰腺内分泌肿瘤患者血浆及肿瘤组织ghrelin水平、血浆瘦素水平,探讨它们之间的关系及临床意义.方法 采用ELISA法检测11例胰腺内分泌肿瘤患者的术前血浆ghrelin及瘦素水平,以28例正常志愿者作为对照.免疫组织化学染色法检测11个肿瘤和27个对照组织ghrelin及其受体GHS-R1A的表达.并与临床病理资料进行相关分析.结果 胰腺内分泌肿瘤患者血浆ghrelin水平为(16.0±5.0)pg/ml,显著低于对照组的(21.0±2.0)pg/ml(P=0.047);瘦素水平为(0.34±0.03)ng/ml,与对照组的(0.38±0.04)ng/ml无显著差异.肿瘤患者的血浆ghrelin与瘦素水平呈正相关(P=0.015),但与各项临床病理指标均不相关;对照组的血浆瘦素水平与体重指数呈正相关(P=0.002),而肿瘤患者两者不相关.肿瘤组织ghrelin的表达率明显低于对照组织(64%对100%,P=0.004),而GHS-R1A的表达率与对照组无显著差异.肿瘤组织ghrelin和GHS-R 1A的表达与各项临床病理指标均不相关.结论 胰腺内分泌肿瘤表达ghrelin及GHS-R1A,患者血浆ghrelin及瘦素水平发生变化.     

血清高尔基体蛋白73诊断原发性肝癌价值探讨

目的探讨高尔基体蛋白73（GP73）诊断肝癌的价值。方法在肝癌107例、肝硬化53例、肝衰竭患者40例和健康人34例,采用ELISA法检测血清GP73浓度,采用ROC曲线寻找GP73诊断肝癌的最佳截断点,并与AFP进行比较,以评价GP73诊断肝癌的价值。结果原发性肝癌、肝硬化和慢性肝衰竭患者血清GP73水平分别为123.5±22.4ng/ml、108.9±30.3ng/ml和130.3±45.6ng/ml,均显著高于健康对照人群（44.1±38.9ng/ml,P〈0.05）;原发性肝癌、肝硬化和慢性肝衰竭患者血清AFP水平分别为236.6±205.3ng/ml、5.3±5.56ng/ml和53.9±40.40 ng/ml;选择血清GP73最佳截断点为77.4ng/ml,其诊断原发性肝癌的灵敏度为89.6%,特异度为100%,AFP的最佳截断点为35.4ng/ml,其诊断原发性肝癌的灵敏度为64.2%,特异度为100%;原发性肝癌患者血清GP73水平在不同年龄、性别、Edmondson分级和结节数目多寡之间无显著性相差,而在不同肿瘤大小、TNM分期和是否合并肝硬化方面均有显著性差异（P＜0.05）。结论血清GP73诊断肝癌的灵敏度优于AFP,尤其在AFP阴性患者诊断中有一定的意义。     

Expression of IGF-II in early experimental hepatocellular carcinomas and its significance in early diagnosis

AIM: To investigate the serum level and expression of insulin growth factor II (IGF-II) in liver tissues of rats with early experimental hepatocellular carcinomas (HCC) and its significance in early diagnosis. METHODS: Early experimental hepatocellular carcinomas were induced by diethylnitrosamine (DENA) in 180 male SD rats. Another 20 male SD rats served as control. The IGF-II serum level was measured by ELISA. Immunohistochemistry and electron microscopic immunohistochemistry were used to observe the expression of IGF-II in normal and tumor liver tissues and its ultrastructural location in malignant hepatocytes. The expressions of IGF-II in human hepatoma cell lines HepG2, SMMC7721 and human embryonic liver cell line L-02 were measured by immunocytochemistry. IGF-II mRNA level was studied by in situ hybridization. RESULTS: IGF-II was expressed in the cytoplasm of both sinusoidal cells in paracancerous cirrhotic liver tissue and malignant hepatocytes in early experimental HCC tissues. Gold particles were seen on the rough endoplasmic reticulum and the mitochondrion in malignant hepatocytes. IGF-II was expressed in the human hepatoma cell lines. The mRNA level of IGF-II was higher in rat liver tumor tissue than in normal rat liver tissue. The serum IGF-II level of the early experimental HCC group was 34.67+/-10.53 ng.ml(-1) and that of the control group was 11.75+/-5.84 ng.ml(-1). The rank sum test was used for statistical analysis. There was a significant difference between the two groups (P<0.01). CONCLUSION: During the induction of early experimental HCC by DENA, IGF-II may promote hepatocytic proliferation via a paracrine mechanism in the pre-cancerous stage. When hepatocytes are transformed into malignant cells, they may secrete IGF-II and promote malignant cell proliferation by an autocrine mechanism. IGF-II may be a possible biological marker in the early diagnosis of HCC.     

脂多糖在慢性乙型肝炎肝内血管病变中的作用

目的探讨LPS在慢性乙型肝炎肝内血管病变中的作用。方法将120例慢性乙型肝炎患者按肝内血管病变级别分为1、2、3级3组,另设10例大致正常肝组织作为对照组。采用ELISA法定量检测血清LPS水平。采用免疫组化染色法检测肝组织TLR4的表达,采用综合评分法判断结果。结果①健康对照组血清LPS水平较低(0.30±0.13ng/ml)。肝内血管病变1级组血清LPS水平为0.32±0.14ng/ml,与正常对照组比较无明显差异(P>0.05)。而肝内血管病变2级、3级组血清LPS水平分别为0.71±0.14ng/ml,1.10±0.15ng/ml,明显高于正常对照组(P<0.01)。慢性乙型肝炎患者血清LPS水平与肝内血管病变严重程度呈正相关(r=0.892,P<0.01)。②不同肝内血管病变级别的慢性乙型肝炎肝组织TLR4阳性表达与对照组比较均有差异(P<0.05)。TLR4主要表达在胞膜上及部分胞浆内,细胞核无表达。TLR4在慢性乙型肝炎肝组织的表达强度与肝内血管病变分级呈正相关(r=0.728,P<0.01)。结论 LPS及其受体TLR4在慢性乙型肝炎肝内血管病变中起着重要作用。血清LPS水平可作为判断肝内血管病变程度的指标之一。     

Expression and regulation of adipocyte fatty acid binding protein in granulosa cells and its relation with clinical characteristics of polycystic ovary syndrome

Increased expression of adipocyte fatty acid binding protein (FABP4) is associated with type 2 diabetic, high triglycerides, increased lipid peroxidation, and inflammation markers. To study the expression of FABP4 mRNA in granulosa cells of patients with polycystic ovary syndrome (PCOS) and the impact of testosterone, insulin, and PPARγ agonist rosiglitazone on granulosa cells (GCs), and to investigate the relationship of serum FABP4 levels with clinical characteristics in patients with PCOS. The expression of FABP4 mRNA in GCs of patients with PCOS and normal controls were assayed by RT-PCR. We assessed the level of FABP4 mRNA after treatment with testosterone, insulin, and rosiglitazone in GCs from normal controls. Serum FABP4 were assayed from 96 patients with PCOS (obese and nonobese 48 cases, respectively) and 80 healthy normal controls (obese and the nonobese 40 cases, respectively). The expression of FABP4 mRNA was higher in the GCs of PCOS than that of the controls (P<0.05). FABP4 mRNA expression was up-regulated by testosterone, insulin, and rosiglitazone at different dosages. Serum FABP4 levels were higher in the nonobese PCOS group than that of the nonobese controls (8.9±5.1 ng/ml vs. 4.8±0.7 ng/ml), and in the obese PCOS group than that of the obese controls (28.2±14.0 ng/ml vs. 15.6±6.6 ng/ml), respectively (P<0.05). Multiple linear regression analyses showed that serum FABP4 level was independently associated with HOMA-IR, BMI, and testosterone (P<0.05). Increased FABP4 was related to the clinical characteristics of PCOS.