瘦素对脂肪细胞的直接调节作用

目的:观察瘦素对人脂肪细胞分解代谢及脂肪蓄积的直接影响,探讨脂肪细胞的自分泌调节作用。方法:取正常成人皮下脂肪组织,常规提取和培养前脂肪细胞,待细胞融合后诱导分化为成熟脂肪细胞并随机分为四组:正常对照组、低浓度组、中浓度组和高浓度组,分别培养于含瘦素浓度为0ng/ml、10ng/ml、100ng/ml、1000ng/ml的培养液a中。培养4h后收集培养液检测游离脂肪酸和甘油浓度,取脂肪细胞经油红O染色后图像分析计算脂肪颗粒的积分光密度。结果:与对照组相比,低浓度组培养液中游离脂肪酸和甘油浓度分别增加87%(P<0.01)和5%(P<0.01),脂肪颗粒积分光密度减少12%(P<0.01);中浓度组培养液中游离脂肪酸和甘油浓度分别增加181%(P<0.01)和8%(P<0.01),脂肪颗粒光密度减少21%(P<0.01);高浓度组培养液中游离脂肪酸和甘油的浓度分别增加312%(P<0.01)和17%(P<0.01),脂肪颗粒的积分光密度减少35%(P<0.01)。游离脂肪酸和甘油浓度与瘦素浓度呈正相关,脂肪颗粒积分光密度与瘦素浓度呈负相关。结论:瘦素瞬时作用脂肪细胞,可促进脂肪分解代谢、减少脂肪蓄积;且随着瘦素浓度增加,作用更强,呈剂量依赖性。瘦素对脂肪细胞存在自分泌调节作用,可能在肥胖发病机制中起重要作用。     

瘦素对人前脂肪细胞增殖及分化的影响

目的 观察瘦索在体外对人前脂肪细胞增殖和分化的影响,探讨瘦素调节肥胖发生的可能机制.方法 分离并体外培养人腹部皮下前脂肪细胞.采用3-（4,5-二甲基噻唑-2）-2,5-二苯基四氮唑溴盐（MTT）比色法、细胞计数法、油红O染色提取法及逆转录-聚合酶链式反应（RT-PCR）方法 分析不同浓度（0～1 000 ng/ml）瘦素对人前脂肪细胞增殖、脂质积聚及分化转录因子γ2过氧化物酶体增殖物激活受体（PPAR-γ）、CCAAT增强子α结合蛋白（C/EBP-α）mRNA表达的影响.结果 高浓度（1 000 ng/ml）瘦素能够促进人前脂肪细胞的增殖、脂质积聚以及PPAR-γ2、C/EBP-α mRNA表达（P〈0.05）.低浓度（10 ng/ml）和中浓度（100 ng/ml）瘦素对人前脂肪细胞的增殖及脂质积聚没有明显的促进作用（P〉0.05）.结论 在体外超生理浓度的瘦素能够促进前脂肪细胞的增殖和分化,提示瘦素抵抗、血清高瘦素浓度等病理状态时,瘦素可能促进前脂肪细胞的增殖及分化,影响肥胖发生.     

富马酸二甲酯对小鼠肾缺血再灌注损伤的保护作用及其机制

目的探讨富马酸二甲酯(DMF)在小鼠肾脏缺血再灌注损伤中的保护作用及可能的机制。方法将小鼠随机分成3组(n=8):假手术组(S组)、缺血再灌注组(IR组)和DMF预处理组(DMF组)。IR组及DMF组制备肾脏IR模型,再灌注24h后收集血清及肾组织,测定血清肌酐(SCr)及尿素氮(BUN)值;评定肾脏组织形态学改变;检测肾脏组织中丙二醛(MDA)含量及超氧化物歧化酶(SOD)活力;Western-blot检测各组肾组织内核因子E2相关因子2(Nrf2)及血红素氧化酶-1(HO-1)蛋白含量。结果IR组SCr及BUN显著高于S组[(143.17±14.18)μmol/L,(26.52±3.56)mmol/L vs.(24.50±5.54)μmol/L,(8.25±2.14)mmol/L,P0.01];DMF组SCr及BUN均低于IR组[(81.83±9.39)μmol/L,(18.62±2.75)mmol/L vs.(143.17±14.18)μmol/L,(26.52±3.56)mmol/L](P0.01);和IR组比较,DMF组的组织形态学损伤较轻(P0.01);DMF组过氧化损伤指标MDA水平低于IR组[(3.55±0.48)μmol/g vs.(5.48±0.70)μmol/g](P0.01),而抗氧化酶SOD水平高于IR组[(35.02±4.13)kU/g vs.(23.80±4.36)kU/g](P0.01)。Western-blot及免疫组化结果显示DMF组Nrf2和HO-1蛋白表达水平高于IR组(P0.05)。结论 DMF对小鼠肾缺血再灌注损伤具有保护作用,其机制可能与激活Nrf2/HO-1通路进而提高肾脏抗氧化应激能力有关。     

双酚A对大鼠睾丸支持细胞糖代谢的影响

目的:观察不同浓度双酚A(BPA)对原代培养大鼠睾丸支持细胞(SC)糖代谢及乳酸脱氢酶(LDH)表达的影响,探讨BPA致男性不育的机制。方法:采用两步酶消化法分离雄性Wistar大鼠睾丸SC,建立SC原代培养模型,免疫组化鉴定Fas L。传代后SC随机分为对照组和实验组(100 nmol/L、10μmol/L和1 mmol/L BPA)。培养48 h后,CCK-8法测定细胞增殖活性,核磁共振波谱法测定细胞内代谢物浓度,RT-PCR及Western印迹检测LDH的表达。结果:体外分离培养SC的纯度为(96.05±1.28)%(n=10),CCK-8实验结果显示:与对照组相比,暴露于100 nmol/L BPA组[(98±8)%]、10μmol/L BPA组[(96±3)%]和1 mmol/L BPA组[(95±3)%]的细胞增殖率无明显变化(P0.05);核磁共振波谱显示:与对照组相比,10μmol/L和1 mmol/L BPA作用下SC内葡萄糖及乳酸浓度明显降低(P0.05);RT-PCR及Western印迹结果显示:LDH mRNA的表达随BPA浓度升高呈现降低趋势(100 nmol/L、10μmol/L及1 mmol/L组P均0.05),而LDH蛋白的表达只在1 mmol/L组明显降低(P0.05)。结论:较高浓度BPA降低LDH,影响SC糖代谢过程。推测BPA通过影响SC糖代谢,减少向生殖细胞乳酸的供给,影响精子发生过程。     

透析液碳酸氢根浓度对透析中血清钾离子浓度的影响

目的 分析使用不同碳酸氢根(HCO3)浓度透析液对慢性维持性血液透析患者透析过程中血清钾离子(K+)浓度下降程度的血液动力学影响.方法 8例稳定血液透析患者进入临床试验,采取双盲、随机、3阶段、交叉对照的设计方案,透析液碳酸氢根浓度制定为:低浓度透析液(LB,27mmol/L)、标准浓度透析液(SB,35 mmol/L)、高浓度透析液(HB,39 mmol/L),每次透析过程血流量均为300 ml/min,透析液流量为500 ml/min,分别在0(基础值)、15、30、60和240 min从透析管路动脉端留取血标本做血液生化检测和血气分析.对血液透析后1 h的血清K+浓度以及通过透析K+的清除量进行检测.每例患者完成3次检测,每次试验检测过程中有1周的实验间期.结果 在低浓度透析液组(LB组),K+浓度从[(5.4±0.26)mmol/L,基础值在15、30、60和240min时分别下降至(4.89±0.25)mmol/L、(4.89±0.22)mmol/L、(4.54±0.25)mmol/L和(4.26±0.44)mmol/L;在标准浓度透析液组(SB组),K+浓度从[(5.38±0.29),基础值]mmo/L在15、30、60和240min时分别下降至(4.89±0.24)mmol/L、(4.43±0.22)mmol/L、(4.08±0.23)mmol/L和(3.90±0.30)mmol/L;在高浓度透析液组(HB组),K+浓度从[(5.38±0.23)mmol/L,基础值在15、30、60和240 min时分别下降至(4.71±0.38)mmol/L、(4.38±0.33)mmol/L、(3.72±0.34)mmol/L和(3.32±0.16)mmol/L,其中高浓度与低浓度和标准浓度(HCO3)在60和240 min时点比较差异有统计学意义(P＜0.05);除了LB组,其他两组中血清K+浓度和HCO3比较差异有统计学意义(P＜0.05);对于LB组、SB组和HB组透析液,血清K+浓度的反弹率分别为(4.0±9.2)%、(5.2±3.2)%、(7.2±3.4)%.每次透析K+的清除量LB组为119.5±22.6(mmol/L)、SB组为85.5±14.9(mmol/L)、HB组为95.6±15.5(mmol/L).结论 高浓度透析液与在透析过程中血清K+的快速清除相关,该清除过程是因为加强了K+从细胞外移至细胞内的过程,而不是通过透析本身对K+的清除.     

三氧化二砷对小鼠肝脏祖细胞生物学特性的影响

目的 观察三氧化二砷(As2O3)对小鼠肝脏祖细胞(AHPCs)增殖及代谢的影响.方法 应用改良Seglen二步法原位灌注结合机械离心获取AHPCs,体外培养并持续观察超过40 d.应用免疫荧光技术对AHPC及其形成的克隆进行白蛋白、甲胎蛋白(AFP)和细胞角蛋白19 (CK19)染色.取原代培养12d的细胞随机分为3组:对照组(不含As2O3)、低浓度组(含2μmol/L As2O3)和高浓度组(含4 μmol/L As2 O3).干预48 h后,采用免疫荧光法观察细胞核增殖抗原(Ki-67)阳性细胞所占的比例,逆转录-聚合酶链反应(RT-PCR)技术检测Ki-67基因的表达,Western blot技术检测增殖细胞核抗原(PCNA)蛋白的表达.酶联免疫吸附试验(ELISA)检测细胞上清液中尿素浓度的变化.结果 体外培养的AHPC可持续扩增超过40 d,培养第1天强阳性表达白蛋白,培养第5天细胞克隆开始表达AFP,第35天表达CK19.阴性对照组所含Ki-67阳性细胞的比例较高(25.1±2.8)％,而As2O3(2μmol/L)组[(18.8±1.0)％]和As2O3(4μmol/L)组[(11.8±2.0)％]的Ki-67阳性细胞比例逐渐降低.Ki-67 mRNA的表达量在As2 O3(2μmol/L)组(0.823 ±0.012)明显下降,并以As2O3(4μmol/L)组(0.309 ±0.002)降低最为明显.随着As2O3浓度的增加,PCNA表达逐渐下降,并呈剂量-效应关系.阴性对照组细胞代谢产物尿素浓度较高[(0.586 ±0.056) mmol/L]随着As2O3浓度增加As2O3(2μmol/L)组[(0.506±0.058) mmol/L]与As2O3 (4 μmol/L)组[(0.410±0.045) mmol/L]尿素浓度逐渐下降.结论 成功建立AHPC体外培养模型.As2O3能抑制原代AHPC的增殖,并降低其代谢能力.     

二种不同治法对甲减肾损害大鼠血管内皮生长因子表达及肾功能形态的影响

目的:主要观察扶正软坚和温肾助阳二种不同治法对甲减肾损害大鼠血管内皮生长因子(VEGF)表达及肾功能形态的影响。方法:将大鼠随机分为正常组及实验组,实验组随机分为模型组、补中益气汤组、芪贝复元饮组,实验组建立碘缺乏致甲减肾损害模型,21d成模时及用药56d后观察甲功(TT3、TT4、TSH)和血清尿素氮(BUN)、肌酐(Scr)水平和肾脏形态及VEGF表达的变化。结果:用药56d后:(1)补中益气汤组血清BUN及Scr与正常组相比差异无统计学意义[(4.87±0.27)mmol/L对(5.00±0.24)mmol/L,(23.81±2.83)μmol/L对(22.5±2.07)μmol/L,P>0.05]。芪贝复元饮组血清BUN及Scr明显高于正常组[(6.42±0.87)mmol/L对(5.00±0.24)mmol/L,(28.0±2.37)μmol/L对(22.5±2.07)μmol/L,P<0.01]。(2)肾脏VEGF光密度:仅芪贝复元饮组小于正常组(4.98±1.99对6.60±2.14,P<0.05),补中益气汤组明显高于模型组(7.79±2.82对5.31±2.09,P<0.01)。(3)PAS染色比较:21d成模时模型组系膜轻度增生,处理56d时模型组轻至中度增生,有部分毛细血管扩张,用药组以芪贝复元饮组增生最重,毛细血管扩张明显,基底膜增厚,补中益气汤组增生最轻,毛细血管开放良好。结论:补中益气汤能够促进肾脏VEGF分泌并且对甲减的肾脏功能、形态恢复都优于芪贝复元饮,温肾健脾法是治疗甲减的首选方法。     

经下腔静脉逆灌注对肝移植大鼠早期肾功能的影响

目的 观察经下腔静脉逆灌注对自体原位肝移植大鼠早期肾功能的影响.方法 将70只自体原位肝移植SD大鼠按肝脏的灌注方式不同随机分为经下腔静脉逆灌注组与经门静脉正灌注组,各组35只.各组再随机分成术前对照组、术后6、12、24、48h5个亚组,各亚组7只.经下腔静脉逆灌注组:先开放下腔静脉,再同时开放门静脉与肝动脉；经门静脉正灌注组:先开放门静脉,再依次开放下腔静脉、肝动脉.分别检测两组中各亚组的血清肌酐( Scr)、尿素氮(BUN)、肾损伤分子(KIM)-1及肿瘤坏死因子(TNF)-α水平；取各亚组左肾组织行光镜检查,观察肾组织KIM-1免疫组织化学,计算KIM-1阳性细胞计数.结果 两组术前Scr、BUN、KIM-1及TNF-α比较差异无统计学意义(P＞0.05).与正灌注组比较,术后6、12及24 h逆灌注组的Scr、BUN及TNF-α水平显著降低[术后6h,Scr:(57.4±14.2) mol/L比(48.0±14.0) mol/L,BUN:(14.1±1.5) mmol/L比(8.0±1.1)mmol/L,TNF-α:( 330.1±11.6) ng/L比(294.5±16.2) ng/L;术后12 h,Scr:(125.0±40.4) mol/L比(105.4 ±40.6) mol/L,BUN:(32.2±2.8)mmol/L比(19.6±2.1)mmol/L;TNF-α:(503.6 ±46.6)ng/L比(261.8±9.1)ng/L;术后24h,Scr:(57.8±12.6)mol/L比(45.4±11.8) mol/L,BUN:(16.4±3.0) mmol/L比(13.6±3.2) mmol/L,TNF-α:(408.2±20.9) ng/L比(226.0±21.1) ng/L]；术后48 h差异无统计学意义(P＞0.05)；术后6、12、24、48 h逆灌注组血清KIM-1水平均显著降低[术后6h,(107.8±2.1)ng/L比(87.3±1.3)ng/L;术后12 h,(107.8±2.1)ng/L比(87.3±1.3) ng/L;术后24 h,(101.7±1.8)比(81.9±1.6) ng/L;术后48 h:(99.7 ±2.6) ng/L比(77.5±0.6)ng/L;P ＜0.05],肾组织中KIM-1阳性细胞计数及免疫组织化学评分显著降低(术后6h,40±3比26 ±2;术后12h,45 ±3比31 ±3;术后24 h,56 ±4比35±4；术后48 h:60±3比32±2;P＜0.05).结论 经下腔静脉逆灌注可减轻SD大鼠自体原位肝移植术后早期肾功能的损害.     

丝裂原活化蛋白激酶信号通路在肝细胞生长因子促进人结肠癌细胞增殖移行中的作用

目的 观察丝裂原活化蛋白激酶(MAPK)信号通路在肝细胞生长因子(HGF)促进人结肠癌细胞SW620增殖、移行中的作用.方法 在细胞培养液中加入MAPK通路中丝裂原细胞外激酶(MEK1/2)的拮抗剂U0126(终质量浓度分别为0.5、1.0、2.0、4.0、8.0 μmol/L),之后加入终质量浓度为20 μg/L的HGF.用噻唑蓝(MTT)比色法检测SW620细胞增殖,流式细胞术检测细胞周期,划痕试验检测移行.二甲基亚砜(DMSO)组加终质量浓度为0.1％体积浓度的DMSO,加入同体积的培养液作为对照组.结果 (1) U0126与20 μg/L HGF共同作用SW620细胞48 h后,低浓度(0.5、1.0、2.0 μmol/L)U0126组、DMSO组与对照组之间比较差异无统计学意义(P＞0.05),当U0126浓度≥4.0μmol/L时能抑制HGF促SW620增殖,但未表现出浓度依赖性.4.0、8.0 μmol/LU0126组增殖抑制率分别为24.6％和28.4％ (P ＜0.05).(2)2.0、4.0、8.0 μmol/L U0126组G1期细胞数增多,而S期细胞数减少,3组的增殖指数(32.32±6.64、23.87±4.88、20.28±5.22)均低于对照组,P＜0.05),且4.0、8.0μmol/L U0126组与2.0 μmol/L组差异有统计学意义(P＜0.05).(3)加入U0126 24 h后,仅8.0μmol/L组SW620细胞移行受到明显抑制,抑制率为60.9％(P＜0.05),DMSO组、4.0mol/L U0126组与对照组移行距离差异无统计学意义(P ＞0.05);48、72 h后,8.0 μmol/L和4.0μmol/L U0126组细胞移行均受到抑制(P＜0.05),48 h抑制率分别为46.5％、61.8％,72 h抑制率分别为44.2％、54.3％,但8.0μmol/L组与4μmol/L组细胞移行距离差异无统计学意义(P＞0.05).结论 MAPK信号通路参与了HGF促人结肠癌细胞SW620增殖和移行的作用.     

琥珀酸对人外周血中性粒细胞凋亡的影响

目的 了解琥珀酸对人外周血中性粒细胞(PMN)凋亡的影响,探讨其致病机制.方法 体外孵育PMN,将PMN浓度调至5×106个/ml.在细胞中加入琥珀酸刺激,根据所加琥珀酸浓度分为5、10、20、30 mmol/L琥珀酸组;对照组加入常规培养液.取各组细胞培养上清液,检测其活性氧含量.5、20 mmol/L琥珀酸组细胞于处理前及处理后2、4、6、8、10 h分别取细胞悬液1 ml,行半胱氨酸天冬氨酸蛋白酶3(caspase-3)活性及细胞凋亡率检测.结果 5、10、20、30 mmol/L琥珀酸组活性氧含量(0.437±0.056、0.432±0.024、0.395±0.049、0.386±0.010)均低于对照组(0.505±0.028,P＜0.05).随着孵育时间延长,各组细胞caspase-3活性均逐渐增加,但与对照组比较,5 mmol/L琥珀酸组caspase-3活性降低,20 mmol/L琥珀酸组则升高(P＜0.05).对照组细胞处理前凋亡率为(6.1±1.1)%,处理后2 h为(13.2±2.0)%,10 h达(27.7±3.7)%;5 mmol/L琥珀酸组细胞凋亡率除处理后4 h外其余时相点均低于对照组(P＜0.05);20 mmol/L琥珀酸组细胞处理后4～10 h凋亡率均高于对照组(P＜0.05).结论 低浓度琥珀酸抑制PMN凋亡,而高浓度琥珀酸可促进PMN凋亡.细菌感染时,通过代谢产物琥珀酸抑制PMN免疫功能.     

瘦素及其受体在胃癌中的表达

目的研究瘦素(Leptin)和瘦素受体(ob-R)在胃癌组织中的表达并探讨其在胃癌发生、发展过程中的作用。方法采用免疫组织化学染色方法检测54例胃癌组织中瘦素和瘦素蛋白的表达。并就其表达与临床病理组织学参数之间的关系进行了相关性分析。结果54例胃癌组织中瘦素和瘦素受体的的表达率为72．22％(39／54)和74．07％(40／54)，肠型胃癌瘦素表达率明显高于弥漫性胃癌。瘦素的表达率与肿瘤组织分化、癌肿大小、转移、TNM分期有关。结论瘦素和瘦素受体以双重表达方式存在于胃癌组织中，参与胃癌的早期发生过程并在其发展中起一定作用。     

Mutations in the human leptin and leptin receptor genes as models of serum leptin receptor regulation

A part of serum Ob leptin, an adipocyte-secreted peptide, is bound to a soluble Ob receptor (sObR). Immunoreactive sObR was measured in 125 lean or obese control subjects (group 1), 18 individuals with a mutation in the leptin gene impairing leptin secretion (group 2), and 10 individuals with a mutation in the ObR gene, leading to production of a truncated ObR not anchored to cell membranes (group 3). In group 1, sObR levels were negatively correlated with age and BMI in children and with BMI in adults. sObR levels were also negatively correlated with leptin levels. Leptin binding activity and sObR levels coeluted in gel-filtration chromatography. In group 2, sObR levels did not differ from those in lean control subjects and were not correlated with BMI. A single peak was detected in chromatographic fractions. In group 3, sObR levels were high and positively correlated with BMI. Immunoreactive sObR coeluted with leptin binding activity. These data demonstrate that leptin is not needed for ObR gene expression, and they suggest that leptin plays a role in receptor downregulation because sObR levels are negatively correlated with leptin levels and BMI in control subjects, whereas sObR levels are not depressed in obese leptin-deficient or leptin receptor-deficient individuals.     

瘦素及瘦素受体在乳腺癌中的表达及临床意义

目的 探讨瘦素及其受体mRNA及蛋白的表达在乳腺癌发生、发展中的意义。方法 采用巢式逆转录-聚合酶链反应〈RT-PCR）和免疫组织化学方法检测39例乳腺癌及其周围正常乳腺组织瘦素及其受体的mRNA及蛋白表达，分析乳腺癌组织瘦素与瘦素受体表达的相关性及其与临床病理之间的关系。结果 瘦素mRNA及蛋白在正常乳腺及乳腺癌组织阳性表达率均为100．00％；瘦素受体mRNA和蛋白在乳腺癌组织阳性表达率为74．40％。正常乳腺组织mRNA阳性表达率7．69％；瘦素及其受体在乳腺癌组织的表达量高于正常组织。差异具有统计学意义（P〈0．01）；瘦素受体的表达与瘦素表达明显相关（P〈0．01）。瘦素及瘦素受体高表达与乳腺癌的转移及浸润明显相关（P〈0．01）。结论 瘦素在乳腺癌的发生发展中可能起着促进作用，瘦素及其受体表达情况可以作为乳腺癌诊断或预后的指标。     

Clinical significance of the leptin and leptin receptor expressions in prostate tissues

Aim： To evaluate the expression of leptin and leptin receptor in benign prostatic hyperplasia （BPH） and prostate cancer （PCa）, and to investigate whether they are associated with the development and progression of PCa. Methods： hnmunohistochemical staining was performed to examine the expression of leptin and leptin receptor in BPH and PCa. PCa was divided into three groups： localized PCa, locally advanced PCa and metastatic PCa. The positive staining was identified and the percentage of the positive staining was graded. We also assessed the relationship between both the Gleason score and body mass index （BMI） and PCa. Results： The percentage of the leptin expression in PCa was significantly higher than that in BPH （P 〈 0.01）. For the PCa group, the expressed levels of leptin showed a considerable correlation with localized PCa and metastatic PCa （P 〈 0.05）. Leptin receptor, however, did not reveal a definite difference between BPH and PCa. The expression of leptin indicated a significant difference between well-differentiated PCa （Gleason score ≤6） and poorly differentiated PCa （Gleason score 8-10） （P 〈 0.05）. The relation between the leptin expression level in PCa and the BMI was not remarkable （P = 0.447）. Conclusion： Our results suggest that leptin might have a promoting effect on the carcinogenesis and progression of PCa.     

瘦素和瘦素受体在食管癌中的表达及其意义

Objective To investigate the role of leptin and leptin receptor in carcinogensis and development of esophageal carcinoma. Methods The expression of leptin and leptin receptor was detected in 52 cases of esophageal carcinoma tissues and 49 cases of normal esophageal tissues by immunohistochemistry. The correlation between their expression and clinicopathological parameters was also analysized. Results The expression rate of leptin and leptin receptor in esophageal carcinoma was 78. 8% (41/52) and 82.7% (43/52) respectively, and the rate in normal esophagus was 58.3% (28/49) and 59.2% (29/49) respectively. The expression rate of leptin and leptin receptor both had statistically significantly differences between esophageal carcinoma and normal esophagus tissues (P ＜ 0. 05). The expression rate of leptin was associated with position, tumor size, differentiation, lymphatic metastasis and TNM stage (P ＜ 0. 05 ). Conclusion Leptin and leptin receptor were dually expressed in esophageal carcinoma.They played important roles in the process of carcinogensis and development of esophageal carcinoma.     

瘦素和瘦素受体在食管癌中的表达及其意义

目的 探讨瘦素及其受体与食管癌发生发展的关系.方法 采用免疫组织化学染色方法检测52例食管癌和49例正常食管组织中瘦素及受体的表达,并分析其与临床病理组织学各参数之间的关系.结果 52例食管癌组织中瘦素与受体的表达率分别为78.8%(41/52)、82.7%(43/52).49例正常的食管组织两者的表达率分别为58.3%(28/49)、59.2%(29/49).瘦素及其受体在食管癌与正常食管组织中的表达差异均有统计学意义(P＜0.05),瘦素及其受体的表达与部位、肿瘤大小、组织学、淋巴结的转移及TNM分期明显相关(P均＜0.05).结论 瘦素及其受体的双重表达在食管癌的发生发展过程中起一定的促进作用.

Abstract：

Objective To investigate the role of leptin and leptin receptor in carcinogensis and development of esophageal carcinoma. Methods The expression of leptin and leptin receptor was detected in 52 cases of esophageal carcinoma tissues and 49 cases of normal esophageal tissues by immunohistochemistry. The correlation between their expression and clinicopathological parameters was also analysized. Results The expression rate of leptin and leptin receptor in esophageal carcinoma was 78. 8% (41/52) and 82.7% (43/52) respectively, and the rate in normal esophagus was 58.3% (28/49) and 59.2% (29/49) respectively. The expression rate of leptin and leptin receptor both had statistically significantly differences between esophageal carcinoma and normal esophagus tissues (P ＜ 0. 05). The expression rate of leptin was associated with position, tumor size, differentiation, lymphatic metastasis and TNM stage (P ＜ 0. 05 ). Conclusion Leptin and leptin receptor were dually expressed in esophageal carcinoma.They played important roles in the process of carcinogensis and development of esophageal carcinoma.     

瘦素和瘦素受体在食管癌中的表达及其意义

Objective To investigate the role of leptin and leptin receptor in carcinogensis and development of esophageal carcinoma. Methods The expression of leptin and leptin receptor was detected in 52 cases of esophageal carcinoma tissues and 49 cases of normal esophageal tissues by immunohistochemistry. The correlation between their expression and clinicopathological parameters was also analysized. Results The expression rate of leptin and leptin receptor in esophageal carcinoma was 78. 8% (41/52) and 82.7% (43/52) respectively, and the rate in normal esophagus was 58.3% (28/49) and 59.2% (29/49) respectively. The expression rate of leptin and leptin receptor both had statistically significantly differences between esophageal carcinoma and normal esophagus tissues (P ＜ 0. 05). The expression rate of leptin was associated with position, tumor size, differentiation, lymphatic metastasis and TNM stage (P ＜ 0. 05 ). Conclusion Leptin and leptin receptor were dually expressed in esophageal carcinoma.They played important roles in the process of carcinogensis and development of esophageal carcinoma.     

Expression of leptin and leptin receptor in the testis of fertile and infertile patients

The aim of our study was to investigate the relationships between the expression of leptin, leptin receptor in the testis and spermatogenesis, and testosterone (T) concentration in infertile men. Testicular tissue samples were collected from the testes of five fertile volunteers, eight patients with obstructive azoospermia (OA), six patients with Sertoli cell-only syndrome (SCO) and 32 oligospermic patients with varicocele testis. In testicular tissue, leptin and leptin receptor were identified by staining with polyclonal antibodies. Serum follicle stimulating hormone, lutenising hormone (LH), and T were determined by chemiluminescence assays. Leptin was expressed on germ cells, mainly on spermatocytes. The ratio of immunostained germ cells to total germ cells was inversely correlated with the concentration of T (r = -0.32, P = 0.01), sperm concentration (r = -0.51, P = 0.002) and Johnsen's score (r = -0.44,P = 0.005). In contrast, leptin receptor immunostained cells were found in the interstitium, primarily in Leydig cells. Leptin receptor expression on Leydig cells was inversely correlated with serum T concentration (r = -0.50, P < 0.001). The dysfunction of spermatogenesis is associated with an increase in leptin and leptin receptor expression in the testis.