门静脉高压症脾功能亢进脾巨噬细胞Toll样受体2、4 mRNA表达变化的研究

目的 检测门静脉高压症(PH)脾亢脾和正常脾巨噬细胞(Mφ)中Toll样受体2、4(TLR2、4) mRNA的表达差异,为进一步深入探讨Toll样受体在PH脾亢发生中的作用奠定基础.方法 选取门静脉高压症脾亢患者(均为慢性乙型肝炎患者)的手术切除脾脏(12例)为实验组,外伤性脾破裂患者的手术切除脾脏(4例)为正常对照组.贴壁培养法分离纯化脾脏组织Mφ,荧光定量PCR法对Mφ表面Toll样受体2、4 mRNA的表达进行检测,并将两组结果进行统计学分析比较.结果 与正常脾脏相比,PH脾亢脾Mφ TLR2、4 mRNA的表达水平明显增强(TLR2:2.29±0.55 vs 1.06±0.53,P <0.05;TLR4:2.32±0.41 vs 1.01±0.14,P <0.01).结论 PH脾亢脾Mφ TLR2、4的mRNA表达水平明显升高,与蛋白水平免疫组化的结果一致,进一步支持了"内毒素血症→脾脏Mφ Toll样受体活化→Mφ吞噬破坏血细胞增多"是PH脾亢发生可能机制的观点.     

肝癌合并脾功能亢进的外科治疗

目的探讨原发性肝癌合并脾功能亢进（脾亢）的外科治疗方法和疗效。方法回顾性研究我院2000年8月至2010年8月41例原发性肝癌合并脾亢手术病例,11例合并重度脾亢患者行肝癌切除及脾脏切除（脾切除组）,其中3例附加贲门周围血管离断术;30例由于中度脾亢采用了肝癌切除及脾动脉结扎术（脾动脉结扎组）。结果术后两组脾亢症状基本消除,脾切除组和脾动脉结扎组术后1周血小板、白细胞均上升,两组间差异无统计学意义（P〉0．05）。脾切除组术后有2例胸腔积液,1例切口感染,3例术后黄疸及腹水并发症,脾动脉结扎组术后腹水2例,1例切口脂肪液化,1例胸腔积液,无手术死亡病例,术后并发症在出院时消失,两组术后并发症发生率差异有统计学意义（P〈0．05）。结论原发性肝癌合并巨脾可行肝切除及脾切除,而有消化道出血史可联合行断流术,手术是安全可行的;而对合并中度脾亢,肝切除合并脾动脉结扎同样近期能达到消除脾亢症状同时减少手术创伤。     

转化生长因子1在不同疾病脾功能亢进患者脾组织中的表达及其意义

目的:探讨转化生长因子β1(TGF-β1)在肝硬化脾功能亢进(脾亢)、血小板减少性紫癜(ITP)脾亢和溶血性贫血脾亢患者脾组织中的表达及其对脾组织纤维化的影响。方法:将脾切除术后的脾脏标本根据病因分为A组(门静脉高压或肝硬化脾亢),B组(ITP脾亢),C组(溶血性贫血脾亢),D组(外伤性脾破裂对照),每组20例。将标本行HE染色和Mason染色作形态学观察,Western blot检测TGF-β1的表达。结果:HE染色和Mason染色可见A,B,C组脾脏均有不同程度的纤维化,其中A组最严重,D组无纤维化。Western blot检测显示TGF-β1在A,B,C组脾组织中的表达均明显高于D组(均P<0.05),而A,B,C各组之间的差异无统计学意义(P>0.05)。结论:脾亢患者脾组织中存在TGF-β1的高表达,可能是导致其脾脏严重纤维化的原因之一。     

门静脉高压症脾亢脾巨噬细胞基因表达谱研究

目的检测门静脉高压症（PHT）脾亢脾和正常脾巨噬细胞的差异表达基因，为从基因水平观察巨噬细胞在门静脉高压症脾亢发生中的作用奠定基础。方法提取门静脉高压症脾亢脾巨噬细胞和正常脾巨噬细胞的总RNA，分别用标有荧光素的dCTP反转录制备cDNA探针，将探针与含有14112点cDNA的Biostar—H140s cDNA表达谱芯片杂交后扫描荧光强度，上述方法重复3次，从而筛选出恒定的差异表达基因。结果3张芯片分别检测到896、1330和898个差异表达基因，恒定的差异表达基因共有121个，占总基因数的0．86％。其中表达上调的已知基因有21个，表达下调的已知基因有73个。差异表达基因涉及离子通道和运输蛋白、细胞周期蛋白类、细胞骨架和运动、细胞受体、细胞信号和传递蛋白、代谢、免疫相关等多个方面。结论筛选出的差异表达基因，对了解脾脏巨噬细胞在门静脉高压症脾亢发生中的作用有重要意义。     

门静脉高压症脾亢脾巨噬细胞数量及其吞噬功能的观察

目的观察门静脉高压症(PH)脾亢脾脏巨噬细胞(MΦ)数量及其吞噬功能的变化,为进一步探讨PH脾功能亢进(脾亢)的发病机制提供依据。方法取20例PH脾亢患者的手术脾脏作为PH组,按脾脏肿大程度的分级标准,再分为中度肿大组(11例)和重度肿大组(9例)。6例正常脾外伤性破裂患者的手术脾脏作为对照组。称重后贴壁法分离培养脾脏MΦ,用细胞计数板在显微镜下计数MΦ的相对数(每g脾脏组织中的MΦ数)并计算MΦ绝对数(整个脾脏内MΦ的总数),鸡红细胞吞噬法计算MΦ的吞噬率和吞噬指数。结果对照组、PH中度和重度脾大组MΦ的相对数分别为(13．13±3．72)×10~5/g、(8．80±0．97)×10~5/g、(7．29±1．33)×10~5/g,PH组比对照组均显著减少(P＜0．01),但PH的两组之间差异无统计学意义(P＞0．05)；PH组脾脏的重量明显增加(P＜0．01),可达正常脾重的3．5～6．0倍(放血后)；各组MΦ的绝对数分别为(1．94±0．55)×10~8、(4．91±1．12)×10~8、(6．86±0．77)×10~8,PH组比对照组均显著增多(P＜0．01),且PH重度肿大组也显著多于中度肿大组(P＜0．01)；各组MΦ的吞噬率和吞噬指数分别为(6,33±0．58)%和(0．07±0．01)、(11．25±2．19)%和(0．14±0．03)、(13．00±2．38)%和(0．16±0．04),PH组比对照组均显著增强(P＜0．01),但PH的两组之间比较差异无统计学意义(P＞0．05)。结论PH脾亢时,脾脏MΦ的相对数虽然减少,但绝对数增多,MΦ的吞噬功能增强。MΦ在PH脾亢的形成中可能扮演着非常重要的角色。进一步支持了脾亢发病中的“脾内阻留学说”。     

不同病因脾切除前后免疫功能变化的研究

作者通过观察正常对照、肝硬变,激素负荷加免疫抑制三组动物模型和临床上外伤性脾破裂、肝硬变脾亢、血液病三组病人脾切除前后免疫功能的变化,发现正常脾脏切除后可导致术后免疫功能下降,但多数可逐步代偿;而肝硬变脾亢和长期应用激素和(或)免疫抑制剂的血液病患者,脾切除前包括脾脏在内的免疫器官已受损害,免疫功能已明显低下,这可能是导致脾切除后感染率较高的主要原因,而切除有免疫障碍的脾脏只是一个次要的因素。     

远端脾肾分流术联合脾部分切除治疗门静脉高压症脾功能亢进疗效探讨

目的 对比研究远端脾肾分流术（Warren术）与远端脾肾分流术联合脾部分切除治疗门静脉高压症脾功能亢进的疗效。方法 选取第四军医大学唐都医院2010年以来22例获得完整随访资料的行外科手术治疗的门静脉高压症脾功能亢进病人,其中Warren术组（分流组）8例,Warren术+脾部分切除组（分流+切脾组）14例,比较观察两组术前、术后第7、30天的外周血象主要指标（白细胞、血小板）以及两组术前、术后第30天外周血免疫指标（IgG、 IgA 、IgM）。结果 Warren术+脾部分切除组病人术后白细胞及血小板恢复指标明显优于Warren术组,差异有统计学意义（P<0.05）;外周血免疫球蛋白检测显示两组术后与术前比较差异无统计学意义（P>0.05）。结论 Warren术联合脾部分切除治疗门静脉高压症脾功能亢进疗效优于单纯Warren术。在有效降低门静脉压力前提下很大程度上解决脾功能亢进,又保留了脾脏正常免疫功能。但切除脾脏比例以及适应证等需根据病人制定个体化治疗方案,尤其在切除脾脏比例方面需要进一步研究验证。     

免疫性血小板减少症脾切除疗效与外周血Th亚群细胞因子表达的关系

目的探讨原发性免疫性血小板减少症（ITP）脾切除血液学疗效与外周血辅助性T细胞（Th）亚群细胞因子的mRNA表达水平的关系。方法采用QuantiGene Plex（QGP）方法,分别检测14例手术有效（R组）和8例手术无效（NR组）的ITP患者腹腔镜脾切除术前后外周血Th1（IL-2、IFN-γ）、Th2（IL-4、IL-5、IL-6、IL-10）、Th3（TGF-β1）、Th17（IL-17）细胞因子的mRNA表达水平的变化。对照组为30例健康体检者。结果术前及术后R组TGF-β1 mRNA的表达水平均明显高于NR组（P值分别为0.001和0.006）及对照组（P值分别为0.001和〈0.001）。术前及术后R组和NR组之间IL-2、IFN-γ与IL-17 mRNA的表达水平差异均无统计学意义。结论脾切除疗效不同的ITP患者TGF-β1的mRNA表达水平存在差异,检测术前TGF-β1的表达水平有助于预测手术疗效。     

肝癌合并门静脉高压脾功能亢进105例的外科个体化治疗

目的：探讨肝癌合并门静脉高压脾功能亢进（脾亢）的外科个体化治疗措施。 方法：回顾性分析中山大学附属第一医院肝胆外科2002年1月至2011年12月10年间收治的105例肝癌合并门静脉高压严重脾亢的患者资料,57例行联合肝脾切除（联合组）,44例行单纯肝癌切除（肝切组）,4例行局部肝癌切除加脾动脉结扎术。 结果：联合组术后1~2周血小板及白细胞均恢复至正常,联合组与肝切组手术平均出血量分别为（903.62±139.24）ml和（802.56±146.52）ml（t = 3.535,P 〈 0.01）,差异有统计学意义,两组并发症分别为14例和15例,差异无统计学意义（χ2 =1.102,P 〉 0.05）,两组围手术期死亡各2例。 结论：联合肝脾切除治疗肝癌合并门静脉高压脾亢可作为首选,只要掌握好适应证,做好围手术期处理,手术是安全的,建立个体化治疗措施是降低术后并发症和死亡率,提高疗效的关键。     

贲门癌根治术中切脾与否对患者免疫功能的影响

目的 探讨切脾与不切脾对进展期贲门癌患者根治术后免疫功能的影响。方法 将进展期贲门癌患者45例随机分为两组：贲门癌根治术联合脾切除（24例）和单纯行贲门癌根治术组（21例）。测定两组患者手术前后的免疫球蛋白（Ig）A、IgM、IgG和C3、C4变化，并进行比较分析。结果 手术前后两组患者体液IgA、IgM、IgG、C3、C4变化差异无统计学意义（P〉0．05）。结论 切除脾脏对贲门癌患者术后免疫功能无明显影响。     

门静脉高压巨脾大部切除后残脾神经分布与定量研究

目的：观察门静脉高压巨脾大部切除后残脾神经纤维分布与密度变化,评估残脾保留的价值。 方法：选取门静脉高压脾肿大行脾大部切除并残脾腹后固定术患者13例,收集患者术后切取的巨脾组织,以及术后8年穿刺获取的残脾组织,另取外伤性脾组织13例为正常对照。采用免疫组化法检测脾神经肽Y（NPY）和神经丝蛋白200（NF 200）阳性神经纤维分布及密度。 结果：3组脾组织NPY和NF200阳性神经纤维的分布部位大致相同,但两者在巨脾组织中的密度明显较高。红髓部分的定量分析显示,巨脾组织NPY与NF200阳性神经纤维密度均明显高于残脾组织和正常脾组织（均P<0.05）,而两种阳性神经纤维密度在残脾组织与正常脾组织间差异无统计学意义（均P>0.05）。 结论：巨脾大部切除术后残脾神经纤维分布及含量与正常脾大致相同,提示解除高压环境后,残脾神经功能能逐渐恢复正常。     

Differential expression of VASP in normal lung tissue and lung adenocarcinomas

BACKGROUND: Vasodilator stimulated phosphoprotein (VASP) is associated with focal adhesions and is thought to have an important role in actin filament assembly and cell motility. We hypothesise that an increase in the expression of VASP is involved in the progression and invasion of lung adenocarcinomas in parallel to tumour progression. A study was undertaken to analyse VASP expression in normal lung tissue and lung adenocarcinomas. METHODS: Human lung tissues with adenocarcinomas (n = 26) were used. Normal lung tissue specimens (n = 14) were taken from areas a standard distance (3 cm) from resected adenocarcinomas of patients who underwent surgical lung resection. Adenocarcinomas were classified according to pathological staging and histopathological grades. Tissues were stained for VASP using immunohistochemistry. RESULTS: Normal lung pneumocytes showed no VASP expression while alveolar macrophages had the strongest immunoreactivity for VASP. Bronchial epithelium (surface epithelium, goblet cells) and bronchial gland cells had a very weak immunoreactivity for VASP. Adenocarcinomas had significantly greater VASP expression than normal epithelium (p < 0.001). Moreover, VASP expression in adenocarcinomas increased significantly with more advanced tumour stage (p < 0.001). CONCLUSIONS: The spatial and differential expression of VASP in normal lung tissue and lung adenocarcinomas suggests that it is likely to be involved in the differentiation of normal lung cells to adenocarcinomas. The significant increase in the expression of VASP in adenocarcinomas in parallel to pathological staging suggests that it may regulate the invasive behaviour of lung adenocarcinomas as adenocarcinoma invasion is increased in more advanced tumours.     

Immunorestorative effects of reimplanted splenic tissue and splenosis

Different immune functions were analysed in detail in 41 patients who had been splenectomized after a traumatic rupture of the spleen within four years after surgical intervention. Patients were assigned to one of the following groups as judged by liver/spleen scintigraphy: (1) patients with reimplanted splenic tissue, (2) patients with splenosis, and (3) patients without splenic tissue. Leukocytosis and an increased number of total lymphocytes as well as B-cells were observed in patients of all groups. In addition, the number of circulating T-suppressor cells was significantly increased in patients with no detectable splenic tissue. In contrast, serum concentrations of immunoglobulins and complement components were in the normal range; similarly, phagocytosis-associated functions of the patients' neutrophils and monocytes were found to be unimpaired (chemiluminescence and particle uptake). However, in all groups of splenectomized patients a deficiency in specific serum opsonic activity against a strain of Escherichia coli (O:102, H:6) could be detected. We conclude that neither splenosis nor autologous reimplantation of splenic tissue restores opsonic deficiency caused by splenectomy.     

Autotransplantation of splenic tissue

Autotransplantation of splenic fragments has already been carried out in humans. The optimal size of the particles and amount of tissue required for this procedure has yet to be found. In normal young pigs and miniature piglets, autologous splenic tissue was transplanted into the greater omentum. The regenerated splenic mass, splenic blood flow, and histology were studied six months later. Implanting small splenic particles produced comparable results to implanting thin slices of splenic tissue. The mass of regenerated splenic tissue was only 3.1 g after implanting the whole spleen and 4.5 g after transplanting half of the spleen, which means 5.3% and 7.8% respectively of the weight of control spleens. The blood flow per gram in the regenerated splenic tissue was much lower than in the normal spleen. The blood flow in the whole of the splenic tissue is important for the clearance function of the spleen. Six months after transplanting the whole or half of the spleen, the blood flow to the regenerated splenic tissue was only 1% of that in the control minipigs. When half of the spleen was left in situ, as a model for a partial splenectomy, and the other half transplanted, the regenerated mass was only 3.4% of all splenic tissue and the blood flow 1.5% of the total splenic blood flow. In this model the regenerated splenic mass was independent of the size of the implants and the mass of implanted tissue. The extremely low blood flow indicates an inadequate clearance function and thus the protective function would probably be negligible.     

Decreased phagocytic capacity of autotransplanted splenic tissue

Background: Asplenic patients have an increased risk of infections. Operations such as autotransplantation have been proposed to restore functional splenic tissue after splenectomy, but the protective value of this tissue is unclear. Immune responses such as production of antibody remain impaired in humans and animals even when such tissue is present, and clearance of particles from the blood is reported to be less efficient than by normal spleen tissue. The present study investigated the phagocytic capacity of cells in the regenerated tissue in vitro, free of the confounding effects of hepatic clearance. Methods: Single cell suspensions were prepared from splenic tissue from rats 6 months after splenic autotransplantation or sham operation. Phagocytosis of killed, fluorescein‐labelled bacteria was measured by flow cytometry. Results: Autotransplanted tissue contained fewer phagocytic cells than normal tissue, and these cells phagocytosed less per cell. Phagocytosis by spleen cells was dependent on heat‐labile opsonic factors. Conclusions: Autotransplanted splenic tissue does not restore the phagocytic capacity lost following splenectomy.     

Differential heparanase-1 expression in malignant and benign pheochromocytomas

INTRODUCTION: Extracellular matrix (ECM) degradation is an essential step that allows tumor cells to penetrate a tissue barrier and become metastatic. Heparanase-1 (HPR) is an endoglycosidase that specifically degrades heparan sulfate proteoglycans, a chief component of the ECM. Previous studies have demonstrated HPR expression in various malignancies and that there is differential HPR expression between benign and malignant tumors. Currently, there is no technique that can reliably predict the malignant behavior of some pheochromocytomas. This study tests whether HPR is differentially expressed in malignant and benign pheochromocytomas. METHODS: Paraffin-embedded specimens from 29 pheochromocytomas were evaluated. The tissues were collected from surgical specimens over a 10-year period from 26 patients (8 males, 18 females) with a mean age of 47 years (range 19-78 years, median 47 years). One female patient underwent 3 separate operations for malignant pheochromocytoma and thus provided 3 specimens. Another female patient had both the primary tumor and a liver metastasis processed, and therefore provided 2 specimens. Patient charts and pathology reports were reviewed to classify the pheochromocytomas as either benign or malignant. Based on clinical behavior and/or pathological evidence of metastasis or invasion into surrounding tissues, 10 specimens were malignant and 19 had benign behavior. As a control, normal adrenal tissue from 3 nephrectomy specimens was included in the study, as was tissue from 1 adrenocortical adenoma. All 33 specimens were tested for HPR gene expression by in situ hybridization (ISH) with an antisense RNA probe and immunohistochemistry (IHC) with an anti-HPR antibody. Statistical analysis was done using the chi(2) test of proportions to determine if HPR expression correlated with malignancy using ISH, IHC, or both tests together. RESULTS: Using ISH, the percentage of HPR expression in the malignant pheochromocytomas was 50% while HPR expression in the benign tumors was 21% (P = 0.11). Using IHC, the percentage of HPR expression in the malignant pheochromocytomas was 80% while HPR expression in the benign tumors was 32% (P = 0.01). Considering both tests cumulatively, all 10 malignant pheochromocytomas stained positive for HPR by ISH and IHC, while only 37% of the benign tumors were positive for HPR expression (P = 0.001). The one adrenal adenoma and the 3 normal adrenal glands processed stained negative for HPR expression by both ISH and IHC. CONCLUSIONS: HPR expression is higher in malignant pheochromocytomas than in benign pheochromocytomas or normal tissue. HPR may contribute to the invasive characteristics of malignant pheochromocytomas and might be used as a marker to distinguish malignant from benign pheochromocytomas. HPR expression might also be used as a prognostic tool in guiding long-term patient follow-up.     

Experimental study on function of regenerated splenic tissue after splenic autotransplantation

To prevent postsplenectomy overwhelming sepsis, splenic autotransplantation has been clinically attempted. However, function of regenerated splenic tissue after splenic autotransplantation has not been completely understood. Changes in weigh of regenerated splenic tissue, splenic blood flow, splenic immune responses and phagocytic function were studied for one year after splenic autotransplantation using Sprague-Dawley rats. At one year after autotransplantation, the weight of regenerated splenic tissue was increased to 80% of the originally implanted spleen and the blood flow was increased to 80% of the control spleen. The counts of lymphocytes and macrophages in the regenerated splenic tissue were significantly low at eight weeks after transplantation, however lymphocytes was increased to 58.8% and macrophages was increased to 29.5% of the control spleen at 16 weeks after transplantation. The blast formation of splenic lymphocytes was lower at the early stage after transplantation, thereafter, it was increased at the later time after transplantation. Microangiography of the regenerated spleen showed new capillaries around the implanted tissue 2 weeks after transplantation. These results suggested that the transplanted splenic tissue was regenerated to the similar structure to normal spleen and immunological function was recovered close to the normal splenic tissue.     

Splenic resection or heterotopic transplantation of splenic tissue as alternatives to splenectomy. Regeneration and protective effect against pneumococcal septicemia

In 82 male Sprague-Dawley rats, divided into eight groups according to surgical procedure performed (total splenectomy, sham operation and six different modes of splenic conservation), resistance to intravenous injection of 4 X 10(3) CFU of Streptococcus pneumoniae type I was evaluated 16 weeks after the surgical procedures. Significant regeneration of the spleen and almost normal resistance to pneumococci was seen 16 weeks after a two-thirds resection. Pieces of the spleen, implanted subcutaneously or into the greater omentum, also showed marked regeneration; though survival time was prolonged, the mortality among these animals following injection with pneumococci did not, however, differ from that of totally splenectomized animals. Dispersed splenic tissue, injected subcutaneously, intramuscularly, or retroperitoneally, showed less sign of regeneration and had no effect on mortality or survival time in partially vis-à-vis totally splenectomized rats.     

Immune cell subpopulations in regenerated splenic tissue in rats.

BACKGROUND: Asplenic patients have an increased risk of infections. Operations such as autotransplantation or splenic artery ligation have been suggested to ensure retention of functional splenic tissue after splenectomy, but their protective value is unclear. Immune responses, such as production of antibody, remain impaired in humans and animals even when such tissue is present, and phagocytosis is less efficient than by normal spleen tissue. In the present study the cellular composition of regenerated tissue is determined. METHODS: Splenic tissue was obtained from rats 6-9 months after splenic autotransplantation, splenic artery ligation or sham operation. The lymphocyte and macrophage subpopulations were labelled using a panel of monoclonal antibodies and analysed by flow cytometry. RESULTS: Both the total number of cells and the number of cells per gram of tissue were significantly reduced. There was a substantial reduction in the percentage of some of the cells examined (CD4+ and CD8+ T lymphocytes subsets), but not all (B lymphocytes, ED1+ and ED2+ macrophages, OX2+ and OX6+ cells). CONCLUSIONS: The reduction in the T lymphocyte subsets in regenerated splenic tissue compared with the normal spleen might explain the immunological dysfunction which persists after splenic autotransplantation. The reduction in the number of macrophages may be responsible for the alteration in phagocytic efficiency of regenerated splenic tissue.     

SELENBP1在结直肠癌中的表达及其与肿瘤分化的关系

目的：通过蛋白质组学技术筛选出结直肠癌（CRC）组织中差异表达最显著的蛋白，并探讨其与CRC疾病特征的关系。方法：收集83例CRC患者手术标本，包括患者的CRC组织，正常大肠黏膜组织，转移的淋巴结以及部分患者同时长有的大肠良性息肉。用二维差异凝胶电泳（2D DIGE）及基质辅助激光解析飞行时间质谱（MALDI-TOF-MS）对新鲜的CRC与正常黏膜组织以行蛋白质组学分析。找出兴趣蛋白后，用Western blot法在新鲜的CRC与正常黏膜组织，以及不同的CRC细胞株中验证；用免疫组化检测石蜡包埋的CRC、正常黏膜、良性息肉和转移淋巴结组织中该蛋白的表达。用Western blot法检测CRC细胞株在丁酸钠（NaB）诱导分化后该蛋白的表达改变。结果：2D-DIGE分析和MALDI-TOF-MS鉴定结果显示，CRC组织中硒结合蛋白1（SELENBP1）表达丰度比正常黏膜组织明显降低2.54倍（P<0.01）。Western blot示，CRC组织中SELENBP1的表达水平明显低于其配对的正常黏膜组织[（0.76±0.37） vs. (1.46±0.56）]（P<0.001），SELENBP1的表达在CRC细胞株中普遍降低。免疫组化示，SELENBP1的表达评分在CRC组织与正常黏膜组织中分别为1.25±0.78和2.02±0.77，组间差异有统计学意义（P<0.001）；在高、中、低分化的CRC组织中分别为1.75±0.53，1.29±0.41，0.89±0.49，组间差异有统计学意义（P<0.05）；在不同分期的CRC组织间、良性息肉与正常黏膜间、转移淋巴结与其配对的原发癌间，差异均无统计学意义（均P>0.05）。各CRC细胞株经NaB分化诱导后，SELENBP1表达均明显增高（均P<0.05）。结论：CRC组织SELENBP1表达降低，SELENBP1表达降低与CRC低分化程度有关，但与疾病进展及淋巴结转移无关。