MCP-1的表达与动脉粥样硬化

单核细胞趋化蛋白１（ＭＣＰ－１）能趋化单核细胞在内皮下间隙聚集，这是动脉粥样硬化最早期的病变之一，近年研究表明，内皮细胞、平滑肌细胞、单核细胞和巨噬细胞均能表达ＭＣＰ－１。并认为动脉粥样硬化病变早期的内皮细胞和内皮下巨噬细胞是ＭＣＰ－１的主要来源。     

阿托伐他汀对ACS患者PCI术后血清MCP-1、IL-10和hs-CRP水平的影响

目的：探讨阿托伐他汀对经皮冠脉介入术（PCI）术后血清单核细胞趋化蛋白-1（MCP-1）、白细胞介素-10（IL-10）和高敏C反应蛋白（hs-CRP）的影响。方法：62例接受PCI术的ACS患者随机分为两组,分别给予阿托伐他汀20mg（A组,n=31）和10mg（B组,n=31）每日一次口服。于术前及术后24h、1周测定血清hs-CRP、MCP-1和IL-10水平。MCP-1、IL-10检测采用酶联免疫吸附法,hs-CRP采用免疫比浊法。结果：①术后24h两组hs-CRP、MCP-1水平升高（P均〈0．01）;术后1周两组均低于术后24h（P均〈0．01）,B组下降较A组更明显（P〈0．05）。②两组IL-10水平术后24h升高（P〈0．05）;术后1周进一步升高（P均〈0．01）,B组明显高于A组（P〈0．01）。③MCP-1／IL-10比值A组术后24h高于术前（P〈0．05）;术后1周两组均低于术前和术后24h（P〈0．01）,B组较A组下降更著（P〈0．01）。④血清hs-CRP、MCP-1水平和MCP-1／IL-10与阿托伐他汀剂量负相关（P均〈0．01）,IL-10与阿托伐他汀剂量正相关（P〈0．01）。结论：①ACS患者PCI术后24h血清hs-CRP、MCP-1、IL-10水平和MCP-1／IL-10比值均明显高于术前。②术后1周血清hs-CRP、MCP-1水平和MCP-1／IL-10水平降低,IL-10水平显著升高,以20mg组为著。③血清hs-CRP、MCP-1和MCP-1／IL-10与阿托伐他汀剂量负相关,IL-10水平与阿托伐他汀剂量正相关。     

氯沙坦对动脉粥样硬化兔的MCP-1及基因表达的实验研究

为了探讨血管紧张素Ⅱ的Ⅰ型受体(AT1R)拮抗剂氯沙坦(Losartan)的抗动脉粥样硬化(AS)作用及观察其是否能抑制单核细胞趋化蛋白-1(MCP-1)的蛋白及基因表达,我们通过高脂饮食及内皮损伤术建立兔AS模型,一组用Losartan(25mg/kg/d),另一组不用,喂养4个月,观察血管内膜的变化;同时做免疫组化及原位杂交,分别观察MCP-1蛋白及基因的表达。结果发现Losartan治疗组兔主动脉内膜面积及内、中膜面积之比均小于未治疗组,其MCP-1的蛋白及mRNA的表达亦明显减少,表明Losartan可通过抑制MCP-1的产生而具有抗AS作用。     

阿托伐他汀对兔动脉粥样硬化斑块的抑制作用

目的探讨阿托伐他汀对兔动脉粥样硬化斑块的抑制作用及其抗动脉粥样硬化(AS)的可能机制。方法24只大耳白兔随机分为常规饲料组、胆固醇饲料组和高脂饲料加阿托伐他汀组,饲养16周。观察实验前后血清胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL)和体质量的变化,处死动物后取主动脉进行病理学检查,采用免疫组化方法测定主动脉壁细胞黏附分子-1(VCAM-1)阳性表达百分比。结果16周后阿托伐他汀组血清TC和LDL水平明显低于胆固醇饲料组,分别为(23.51±10.58)mmol/L和(14.27±3.51)mmol/L(P<0.01)、(21.39±10.00)mmol/L和(14.23±4.01)mmol/L(P<0.01)。病理学大体观察,对照组、胆固醇饲料组和阿托伐他汀组斑块/内膜面积比分别为0%、(28.12±3.77)%和(16.09±2.77)%,组间比较有显著性差异(P<0.01);光镜下三组内膜厚度分别为(4.45±0.58)μm、(67.47±7.13)μm和(38.11±6.02)μm、内膜/中膜比分别为0.0537±0.007、0.878±0.370和0.391±0.213,组间比较有显著性差异(P<0.01)。免疫组化检测胆固醇饲料组和阿托伐他汀组AS局部VCAM-1的阳性表达百分比明显高于对照组(P<0.01),但阿托伐他汀组较胆固醇饲料组的表达明显减少(P<0.01)。结论阿托伐他汀具有降脂以外的抗AS的作用,抑制VCAM-1的过度表达可能是其抗AS的机制之一。     

IL-8,MCP-1,RANTES与妊娠的研究进展

趋化因子是一类对中性粒细胞、单核细胞、嗜酸性粒细胞等起激活和趋化作用的细胞因子,介导炎症与免疫反应。其中,白细胞介素-8属于趋化因子CXC亚族,单核细胞趋化蛋白-1和正常T细胞活化后所表达和分泌的调节蛋白属于趋化因子CC亚族,它们与妊娠关系密切,在胚胎植入、宫颈成熟、分娩发动中发挥重要作用,其表达异常可导致宫内感染、早产和流产。     

强化阿托伐他汀对老年冠状动脉介入后血清MCP-1、hs-CRP和sFas因子的影响

目的:探讨阿托伐他汀对老年冠状动脉介入治疗术(PCI)后血清单核细胞趋化蛋白1(MCP-1)、高敏C反应蛋白(hs-CRP)和血浆可溶性Fas(sFas)的影响。方法:52例接受PCI的稳定型心绞痛患者随机分为观察组和对照组,对照组予常规治疗;观察组在对照组基础上予口服阿托伐他汀40 mg,qd,治疗4~7 d后行PCI术。于术前及术后24 h、1周测定患者血清MCP-1、hs-CRP和血浆sFas水平。MCP-1、sFas检测采用酶联免疫吸附法,hs-CRP采用免疫比浊法。结果:两组hs-CRP、MCP-1及sFas水平术后24 h升高,术后1周低于术后24 h,观察组较对照组下降更明显,两组差异有统计学意义(P0.05)。结论:老年冠状动脉介入治疗术后应用大剂量阿托伐他汀能促进MCP-1、hs-CRP和sFas水平下降,有利于动脉粥样硬化斑块的稳定,预防再狭窄的发生。     

阿托伐他汀通过下调NLRP1炎性体表达抑制IL-1β和IL-18的释放

 目的:探讨核苷酸结合寡聚化结构域样受体蛋白1(NLRP1)炎性体在阿托伐他汀抑制THP-1巨噬细胞白细胞介素-1β(IL-1β)和白细胞介素-18(IL-18)分泌中的作用。方法:用10 μg/L脂多糖诱导THP-1巨噬细胞分泌IL-1β和IL-18,以不同浓度阿托伐他汀(1、10和20 μmol/L)孵育细胞24 h,或以10 μmol/L阿托伐他汀处理细胞不同时间(12、24和48 h),或转染NLRP1 siRNA以沉默细胞内NLRP1的表达。采用RT-PCR检测细胞内NLRP1炎性体mRNA的表达,Western blot检测细胞内NLRP1炎性体蛋白的表达,ELISA检测细胞上清液中IL-1β和IL-18的含量。结果:阿托伐他汀可抑制THP-1巨噬细胞NLRP1炎性体mRNA和蛋白的表达,且这种效应呈浓度和时间依赖性。转染NLRP1 siRNA后,THP-1巨噬细胞NLRP1的蛋白表达明显下降,且阿托伐他汀对IL-1β和IL-18分泌的抑制作用明显增强。结论:阿托伐他汀通过抑制NLRP1炎性体表达减少巨噬细胞IL-1β和IL-18的释放,发挥抗炎作用,进而延缓动脉粥样硬化进展。     

法舒地尔对大鼠动脉粥样硬化斑块中单核细胞趋化蛋白-1表达的抑制作用

目的探讨Rho/Rho激酶途径在大鼠动脉粥样硬化形成过程中的作用及机制。方法将30只健康雄性Wistar大鼠（体质量220～250g）,随机分为正常对照组、动脉硬化组和法舒地尔组,每组10只。正常对照组行假球囊损伤手术给予正常饮食,余两组每只大鼠给予30万U/kg维生素D3右下肢肌肉注射后用球囊行动脉拉伤,在基础饲料中加入2%胆固醇、0.5%胆酸钠、0.2%丙基硫氧嘧啶、维生素D3粉剂（1.25×10^6U/kg饲料）、3%猪油等饲养。法舒地尔组同时给予法舒地尔5mg/kg体质量,每日2次腹腔注射。喂养9周后空腹24h抽血并处死,检测血脂水平,自主动脉弓下约1cm处留取动脉组织1cm用4%甲醛溶液固定,行HE染色,用免疫组织化学法检测斑块中血管紧张素Ⅱ-1型受体（AT1R）和单核细胞趋化蛋白-1（MCP-1）蛋白的表达。结果动脉硬化组均形成了典型的粥样斑块;免疫组化半定量分析表明：动脉硬化组与正常对照组和法舒地尔组比较,AT1R和MCP-1蛋白均明显升高（P〈0.001）,法舒地尔组与正常对照组比较,AT1R和MCP-1蛋白的表达也明显升高,有明显差异（P〈0.05）。结论Rho/Rho激酶途径在大鼠动脉粥样硬化的形成过程中参与了重要的作用,该途径的激活与RAS系统的激活有密切关系,Rho激酶抑制剂的抗动脉粥样硬化作用可能是通过抑制了MCP-1的表达而起作用。     

IL-6对大鼠血管平滑肌细胞TWEAK受体Fn14表达及功能的影响

目的:观察白介素-6(IL-6)对Wistar大鼠血管平滑肌细胞肿瘤坏死因子样凋亡微弱诱导剂(TWEAK)受体-人成纤维细胞生长因子诱导14(Fn14)表达及功能的影响。方法:将含有不同浓度IL-6(20ng/ml、50ng/ml)的培养液培养平滑肌细胞,用RT-PCR半定量检测各组平滑肌细胞Fn14mRNA的表达,用Westernblot检测各组平滑肌细胞Fn14蛋白的表达。在20ng/mlIL-6组中,用抗Fn14抗体阻断Fn14作用后,用ELISA观察各组血管平滑肌细胞单核细胞趋化蛋白-1(MCP-1)表达的变化。结果:与空白对照组相比,20ng/mlIL-6组和50ng/mlIL-6组Fn14mRNA和蛋白表达均显著升高(P0.01);50ng/mlIL-6组显著高于20ng/ml组(P0.01)。20ng/mlIL-6可显著增加平滑肌细胞表达MCP-1,其水平显著高于抗Fn14单克隆抗体组(P0.05)和空白对照组(P0.01)。结论:IL-6可诱导血管平滑肌细胞表达TWEAK受体Fn14,阻断Fn14的作用可减少IL-6诱导的MCP-1的表达,提示TWEAK/Fn14参与IL-6诱导的动脉粥样硬化形成。     

氧化型α1-抗胰蛋白酶对HBE细胞释放炎症因子的影响

 目的：探讨氧化型α1-抗胰蛋白酶（Ox-AT）对体外培养人支气管上皮(HBE)细胞炎症因子白细胞介素8（IL-8）和单核细胞趋化蛋白1（MCP-1）释放的影响及可能机制。方法：从人血浆中分离纯化获得天然构型AT（N-AT）,加入氧化剂获得Ox-AT;用不同浓度N-AT和Ox-AT分别作用于体外培养的HBE细胞,用ELISA方法检测不同时段培养上清液中IL-8和MCP-1的含量,同时观察NF-κB抑制剂Bay11-7082对Ox-AT引起HBE细胞炎症因子释放的影响。结果：Ox-AT可促进HBE细胞释放IL-8和MCP-1,其促进作用与Ox-AT的浓度及作用时间呈正相关;用0.5 g/L Ox-AT孵育HBE细胞4、10和24 h,其促进HBE细胞分泌IL-8和MCP-1的作用与10 μg/L肿瘤坏死因子 α（TNF-α）的作用基本一致,而 N-AT无刺激HBE细胞分泌IL-8和MCP-1的作用;Ox-AT 能显著增加NF-κB活性; Ox-AT的促炎症作用能被NF-κB抑制剂Bay11-7082抑制。结论：Ox-AT是人正常支气管上皮细胞的强致炎因子,机制可能与NF-κB信号通路激活有关。     

Expression of monocyte chemoattractant protein-1 and interleukin-8 receptors on subsets of T cells: correlation with transendothelial chemotactic potential

The differential expression of chemokine receptors may be an important mechanism for the regulation of T cell migration. To test this, we examined the expression and function of the monocyte chemoattractant protein (MCP)-1 and interleukin (IL)-8 receptors on various populations of T cells. Using a simple and reliable transendothelial chemotaxis assay, both MCP-1 and IL-8 were shown to be chemotactic for subsets of blood T cells, although the relative response varied from donor to donor. To examine receptor expression and correlate it with chemotaxis of T cell subsets, monoclonal antibodies (mAb) to the receptors were produced by immunizing mice either with synthetic peptides (MCP-1 receptor), or with receptor transfectants (IL-8 receptors A and B). A flow cytometric analysis of blood T cells with an anti-MCP-1 receptor mAb revealed low expression on the CD26^hi subset and undetectable expression on other T cells. Staining of T cells with anti-IL-8RA and anti-IL-8RB showed much higher levels of expression, but only on a subset of CD3⁺ cells which were CD8⁺ and CD56^?. That IL-8 and MCP-1 attracted distinct subsets of T cells was best illustrated using the CD26 marker, since IL-8R⁺ T cells were CD26^?, whereas T cells expressing detectable MCP-1R or which responded to MCP-1 in chemotaxis assays were CD26^hi. T cells activated in vitro with anti-CD3 up-regulated expression of the MCP-1 receptor, but not the IL-8 receptors, and were attracted to MCP-1 much more efficiently than resting T cells. These results show that there is a clear distinction between the IL-8- and MCP-1-responsive T cell populations and that chemokine receptor expression on T cells may be regulated with respect to lineage as well as cellular activation.     

载脂蛋白E基因敲除小鼠动脉粥样硬化早期血管外膜成纤维细胞增殖活性增强

目的:探讨动脉外膜成纤维细胞增殖与早期动脉粥样硬化病灶形成的关系。方法:选择6周龄载脂蛋白E基因敲除[apoE(-/-)]小鼠和野生型C57BL/6小鼠,高脂喂养2、4和10周后,在各个时点处死动物前24 h经腹腔注射5-溴-2-脱氧尿嘧啶(BrdU),后选取升主动脉制备连续切片,通过HE染色观察组织形态学的变化,用免疫组化方法观察不同时点血管外膜及内膜BrdU的表达变化。体外培养高脂喂养2周的apoE(-/-)小鼠和C57BL/6小鼠动脉外膜成纤维细胞,通过BrdU掺入法测定细胞增殖活性,流式细胞术测定细胞周期。结果:体内实验发现apoE(-/-)小鼠高脂喂养2周后,在无可见内膜病灶形成之前,首先在主动脉外膜发现BrdU标记的阳性细胞,之后才在损伤内膜观察到BrdU标记细胞。而C57BL/6小鼠在任何时点都未检测到BrdU标记的细胞。体外实验观察到apoE(-/-)小鼠血管外膜成纤维细胞BrdU标记的细胞数显著多于C57BL/6小鼠(P0.01),apoE(-/-)小鼠血管外膜成纤维细胞S期及G2/M期所占百分比明显高于对照组(P0.05)。结论:血管外膜成纤维细胞增殖可能参与早期动脉粥样硬化病灶形成。     

Interleukin-8 and its receptor CXCR2 in atherosclerosis

The participation of inflammatory cells in atherosc lerosis is a well-known process that involves numerous molecules including chemotactic cytokines (chemokines) for their entry into the vessel wall. Although the C-C chemokine monocyte chemoattractant protein-1 and its receptor, CCR2, have been implicated in atherosclerosis, the role of the classic C-X-C chemokine, interleukin-8 (KC/growth-related oncogene α in mice) and its receptor XCCR2 has not been studied in the pathogenesis of atherosclerosis. Our research has shown that CXC R2 is strongly expressed on macrophages (Mф) in atherosclerotic lesion. This CXCR2 expression is proatherogenic in that CXCR2 deficiency significantly reduces the progression of advanced atherosclerosis in mice. Although the mechanism still needs to be worked out, it appears that CXCR2 expression on lesion Mф is essential for these cells to be retained in the lesion.     

HSP22在高脂致动脉粥样硬化病变中的作用及对他汀干预的影响

目的:研究热休克蛋白22(heat shock protein 22,HSP22)在高脂饮食诱导的小鼠动脉粥样硬化(atherosclerosis,AS)病变中的作用,及其对阿托伐他汀(atorvastatin,Ator)干预的影响。方法:8~9周龄Apo E~(-/-)和HSP22~(-/-)Apo E~(-/-)和HSP22+Apo E~(-/-)雄性小鼠各18只,每种小鼠分为2个亚组,分别为对照组与他汀干预组(Ator组),HSP22~(-/-)组(KO组)与HSP22~(-/-)他汀干预组(KO+Ator组)及HSP22~+组(Tg组)与HSP22~+他汀干预组(Tg+Ator组),各干预组从第5周开始给予Ator(10 mg·kg~(-1)·d~(-1))干预,各对照组给予等量生理盐水,共饲养13周。采用油红O及苏木精-伊红(hematoxylin-eosin,HE)染色法观察AS病变程度,免疫组化法、Western blot法和ELISA法检测主动脉和血清中HSP22、NF-κB、eNOS、ICAM-1及IL-6的表达。结果:油红O及HE染色示Tg组主动脉斑块相对面积低于KO组(P0.05)。KO组的血清和主动脉中HSP22的蛋白表达显著低于对照组和Tg组,对照组显著低于Tg组。Tg组及对照组的主动脉eNOS蛋白的表达显著高于KO组。对照组的主动脉NF-κB及ICAM-1蛋白表达较KO组显著降低,较Tg组显著升高。对照组、KO组及Tg组血清IL-6水平的差异无统计学显著性。结论:HSP22基因缺失可上调NF-κB和ICAM-1的表达,降低eNOS的表达,加速AS的进展;HSP22基因过表达可降低NF-κB和ICAM-1的表达,从而改善AS。HSP22基因缺失部分限制了他汀下调NF-κB和ICAM-1及上调eNOS表达的作用;其过表达可促进他汀下调ICAM-1表达,进一步改善AS。     

人胃癌及癌旁组织RNA氧化损伤水平的比较及临床意义

目的:通过检测人胃癌组织及其癌旁组织中的RNA氧化损伤程度,探讨RNA氧化与胃癌发生的相关性。方法:分别利用免疫组化方法和液相-串联质谱(LC-MS/MS)方法对61例胃癌组织及其癌旁组织中8-氧鸟苷(8-oxo Gsn)进行定性和定量分析,并统计分析结果。结果:免疫组化结果检测显示8-oxo Gsn在癌旁组织中含量低,而在胃癌组织中含量明显增高,且棕色染色区域主要集中在肿瘤细胞胞浆位置。质谱检测结果显示胃癌组织中8-oxo Gsn含量较对应癌旁组织高,差异有统计学意义(P0.05)。结论:8-oxo Gsn在胃癌组织中含量增加。RNA氧化损伤可能在胃癌的发生发展过程中起重要作用。     

睾酮双向影响脐静脉内皮细胞分泌单核细胞趋化蛋白1

雄激素与动脉硬化(arteriosc lerosis,AS)的关系日益受到关注,单核细胞趋化蛋白1(monocyte chemoattractant prote in-1,MCP-1)是促进AS的重要炎症介质。本研究以人脐静脉内皮细胞(hum an umb ilical ve in endothelial cell,HUVEC)为对象,观察不同浓度睾酮对MCP-1蛋白表达的影     

Inflammation and atherosclerosis: Cardiovascular evaluation in patients with autoimmune diseases

Evidence now indicates that inflammation contributes considerably to the initiation and progression of atherosclerosis and active inflammatory processes may trigger plaque rupture and enhance the risk of coronary thrombosis leading to a clinical ischemic event. Interest in characterizing inflammatory markers that predict clinical events have dominated clinical investigation. Such markers include C-reactive protein, Fibrinogen and a number of interleukins.Human macrophages avidly phagocytize cholesterol crystals. These cholesterol crystals induce a dose-dependent secretion of mature Interleukin 1-beta (IL-1β) from human monocytes and macrophages (an NLRP3 inflammasome-mediated pathway). Since IL-1β production leads to increased levels of IL-6 and C-reactive protein, this could be a mechanistic link between early deposition of cholesterol crystals within the vessel wall to the macrophage–monocyte interactions that initiate fatty streaks and promote local atherosclerotic progression. We have entered a time where a pure anti-inflammatory drug without significant effects on lipids or any other traditional cardiovascular risk factor decreased cardiovascular events. Patients with autoimmune diseases are at increase cardiovascular risk. In this review we describe the link between inflammation and atherosclerosis. Furthermore we explore the data regarding primary prevention, cardiac imaging for risk stratification and the implications of targeting inflammation in patients with autoimmune disease.     

孕妇IL-8、IL-10血清学水平与早期自然流产的相关性研究

目的探讨细胞因子IL-8及IL-10与早期自然流产的关系。方法应用酶联免疫法对46例先兆流产孕妇、56例难免流产孕妇（观察组）进行静脉血IL-8及IL-10的检测,并以53例正常妊娠妇女作为对照（对照组）。结果流产组孕妇血IL-8水平显著高于对照组,而IL-10水平显著低于对照组,差异均有显著性（P〈0.05）;先兆流产治疗成功组孕妇治疗前、后血IL-8、IL-10差异有显著性（P〈0.01）;先兆流产治疗不成功组孕妇治疗前、后血IL-8、IL-10差异无显著性（P〉0.05）。结论早期自然流产孕妇存在细胞因子IL-8、IL-10异常,IL-8可促进早期自然流产发生,而IL-10在维持正常妊娠中可能起重要作用。     

The effect of COX-2 inhibitor,nimesulide, on angiogenetic factors in primary endometrial carcinoma cell culture

Abstract Angiogenesis, the development of new blood vessels from preexisting capillaries, is essential for the development, growth and advancement of solid tumours. Angiogenesis is enhanced by prostaglandins (PGs) that are synthesised by the catalysis of cyclooxygenases (COX-1 and COX-2) from arachidonic acid. COX-2 is upregulated in a variety of malignancies and favours the growth of malignant cells by stimulating proliferation and angiogenesis. The aim of this study is to investigate the angiogenetic process by determining the levels of vascular endothelial growth factor (VEGF), monocyte chemoattractant protein (MCP)-1 and interleukin (IL)-8 in endometrial cancer cells and to study the effect of nimesulide, a selective COX-2 inhibitor, on these mediators using cell culture. Endometrial tissue specimens were obtained from subjects with endometrial cancer and intramural leiomyoma. Cells were incubated with either 10 or 50 μM nimesulide for 24 h. VEGF, MCP-1 and IL-8 concentrations were determined by sandwich quantitative enzyme immunoassay (ELISA). VEGF concentration was significantly higher in cancer cells than normal endometrial cells. VEGF was decreased with 10 μM nimesulide in cancer cells whereas it remained unaltered in normal cells. Both MCP-1 and IL-8 concentrations were lower in cancer cells than normal cells. MCP-1 levels were decreased with both doses of nimesulide in normal cells, whereas IL-8 levels were significantly affected only by 50 μM of nimesulide. These results suggest that COX-2 inhibitors may be effective in the treatment of endometrial cancer via suppression of angiogenesis.     

肺腺癌巨噬细胞M2表型边缘极化效应观察及预后分析

目的:探讨肺腺癌边缘区巨噬细胞M2表型的极化效应、边缘/中心比值及对预后的影响。方法:采用双重免疫组化技术,观察巨噬细胞CD163+/CD68+表型(M2表型)在49例原位肺腺癌(AIS)、11例微小浸润性腺癌(MIA)、57例浸润性腺癌(IA)边缘区及中心区的分布规律和差异,探讨巨噬细胞边缘极化效应及边缘/中心比值在肺腺癌进程中的作用及机制。采用单因素Kaplan-Meier生存曲线分析及多变量Cox生存分析探讨M2表型边缘极化状态与预后的关系。结果:肺腺癌边缘区M2型巨噬细胞较中心区域呈现极性聚集,具有显著差异(P0.01)。根据中位数分高、低极化组,低极化组AIS中M2型巨噬细胞计数值与MIA及IA比较未见明显差别,但其在高、极化组AIS中的计数值依次低于MIA和IA,差异有统计学意义(均P0.01)。单因素Kaplan-Meier生存曲线分析及log-rank检验结果显示边缘区巨噬细胞M2表型数量及边缘/中心比值与生存时间呈负相关(2=44.71,P0.01;2=21.75,P0.01)。多变量Cox生存分析表明M2表型边缘高极化状态和边缘/中心比值是独立的预后危险因素(P0.01)。结论:巨噬细胞M2表型在肺腺癌边缘区存在边缘极化效应,其边缘极化状态和边缘/中心比值是独立的预后危险因素,因此术前穿刺判断边缘极化状态或术后活检检测M2型巨噬细胞型边缘/中心比值可能是评估预后的一种有效方法。