Portal vein thrombosis with protein C-S deficiency in a noncirrhotic patient

There are several conditions that can lead to portal vein thrombosis(PVT), including including infection, malignancies, and coagulation disorders. Anew condition of interest is protein C and S deficiencies, associated with hypercoagulation and recurrent venous thromboembolism. We report the case of a non-cirrhotic 63-year-old male diagnosed with acute superior mesenteric vein thrombosis and PVT and combined deficiencies in proteins C and S, recanalized by short-term low molecular heparin plus oral warfarin therapy.

Heat shock protein 72 normothermic ischemia,and the impact of congested portal blood reperfusion on rat liver

INTRODUCTIONFrom the technical aspect of liver surgery ,control of bleeding during hepatic parenchymal resection is one of the most important procedures in hepatectomy .Pringle,s maneuver ,a temporary cross-clamping of the hepatoduodnal ligament ,has often been used for this purpose[1],This is the simplest and userul technique to reduce intraoperative blood loss .

Increased endothelin receptor B and G protein coupled kinase-2 in the mesentery of portal hypertensive rats

AIM: To elucidate the mechanisms of mesenteric vasodilation in portal hypertension (PHT), with a focus on endothelin signaling. METHODS: PHT was induced in rats by common bile duct ligation (CBDL). Portal pressure (PP) was measured directly via catheters placed in the portal vein tract. The level of endothelin-1 (ET-1) in the mesenteric circulation was determined by radioimmunoassay, and the expression of the endothelin A receptor (ETAR) and endothelin B receptor (ETBR) was assessed by immunofluorescence and Western blot. Additionally, expression of G protein coupled kinase-2 (GRK2) and β-arrestin 2, which influence endothelin receptor sensitivity, were also studied by Western blot. RESULTS: PP of CBDL rats increased significantly (11.89 ± 1.38 mmHg vs 16.34 ± 1.63 mmHg). ET-1 expression decreased in the mesenteric circulation 2 and 4 wk after CBDL. ET-1 levels in the systemic circulation of CBDL rats were increased at 2 wk and decreased at 4 wk. There was no change in ETAR expression in response to CBDL; however, increased expression of ETBR in the endothelial cells of mesenteric arterioles and capillaries was observed. In sham-operated rats, ETBR was mainly expressed in the CD31+ endothelial cells of the arterioles. With development of PHT, in addition to the endothelial cells, ETBR expression was noticeably detectable in the SMA+ smooth muscle cells of arterioles and in the CD31+ capillaries. Following CBDL, increased expression of GRK2 was also found in mesenteric tissue, though there was no change in the level of β-arrestin 2. CONCLUSION: Decreased levels of ET-1 and increased ETBR expression in the mesenteric circulation following CBDL in rats may underlie mesenteric vasodilation in individuals with PHT. Mechanistically, increased GRK2 expression may lead to desensitization of ETAR, as well as other vasoconstrictors, promoting this vasodilatory effect.

Extrahepatic portal vein thrombosis in children and adolescents:Influence of genetic thrombophilic disorders

AIM:To explore the prevalence of local and genetic thrombophilic disorders as risk factors for portal vein thrombosis (PVT) in our series,the largest ever published in pediatric literature. METHODS:We conducted a case-control study enrolling 31 children with PVT and 26 age-matched controls. All were screened for thrombophilia,including genetic disorders,protein C,protein S and homocysteine deficiencies. All coagulation parameters were studied at least 3 mo after the diagnosis of portal vein obstruction.RESULTS:In our study we showed that most pediatric patients with PVT have local prothrombotic risk factors,which are probably the most important factors leading to PVT. However,there is a clear association between the presence of prothrombotic disorders and PVT,suggesting that these increase the risk of thrombosis in patients with local factors such as perinatal umbilical vein catheterization or sepsis. CONCLUSION:Patients with PVT should be screened for inherited prothrombotic disorders regardless of a history of an obvious local risk factor.

Role of HSP-90 for increased nNOS-mediated vasodilation in mesenteric arteries in portal hypertension

AIM:To explore the role of heat shock protein-90 (HSP-90) for nitrergic vasorelaxation in the splanchnic circulation in rats with and without portal hypertension. METHODS: Neuronal nitric oxide synthase (nNOS) and HSP-90 were analyzed by immunofluorescence, western blotting and co-immunoprecipitation in the mesenteric vasculature and isolated nerves of portal-vein-ligated (PVL) rats and sham operated rats. In vitro perfused de-endothelialized mesenteric arterial vasculature was preconstricted with norepinephrine (EC80) and tested for nNOS-mediated vasorelaxation by periarterial nerve stimulation (PNS, 2-12 Hz, 45V) before and after incubation with geldanamycin (specific inhibitor of HSP-90 signalling, 3 μg/mL) or L-NAME (non-specific NOSblocker, 10-4 mol/L). RESULTS: nNOS and HSP-90 expression was significantly increased in mesenteric nerves from PVL as compared to sham rats. Moreover, nNOS and HSP-90 were visualized in mesenteric nerves by immunofluorescence and immunoprecipitation of nNOS co-immunoprecitated HSP-90 in sham and PVL rats. PNS induced a frequencydependent vasorelaxation which was more pronounced in PVL as compared to sham rats. L-NAME and geldanamycin markedly reduced nNOS-mediated vasorelaxation abrogating differences between the study groups. The effect of L-NAME and geldanamycin on nNOS-mediated vasorelaxation was significantly greater in PVL than in sham animals. However, no difference in magnitude of effect between L-NAME and geldanamycin was noted. CONCLUSION: HSP-90 acts as a signalling mediator of nNOS-dependent nerve mediated vascular responses in mesenteric arteries, and the increased nitrergic vasorelaxation observed in portal hypertension is mediated largely by HSP-90.

Desensitization of G-protein-coupled receptors induces vascular hypocontractility in response to norepinephrine in the mesenteric arteries of cirrhotic patients and rats

BACKGROUND: The increased β-arrestin-2 and its combination with G-protein-coupled receptors (GPCRs) lead to GPCRs desensitization. The latter may be responsible for decreased contractile reactivity in the mesenteric arteries of cirrhotic patients and rats. The present study is to investigate the machinery changes of α-adrenergic receptors and G proteins and their roles in the contractility of mesenteric arteries of cirrhotic patients and animal models. METHODS: Patients with cirrhosis due to hepatitis B and cirrhotic rats induced by CCl 4 were studied. Mesenteric artery contractility in response to norepinephrine was determined by a vessel perfusion system. The contractile effect of G protein-coupled receptor kinase-2 (GRK-2) inhibitor on the mesenteric artery was evaluated. The protein expression of the α 1 adrenergic receptor, G proteins, β-arrestin-2, GRK-2 as well as the activity of Rho associated coiled-coil forming protein kinase-1 (ROCK-1) were measured by Western blot. In addition, the interaction of α 1 adrenergic receptor with β-arrestin-2 was assessed by co-immunoprecipitation. RESULTS: The portal vein pressure of cirrhotic patients and rats was significantly higher than that of controls. The doseresponse curve to norepinephrine in mesenteric arteriole was shifted to the right, and EC 50 was significantly increased in cirrhotic patients and rats. There were no significant differences in the expressions of the α 1 adrenergic receptor and G proteins in the cirrhotic group compared with the controls. However, the protein expressions of GRK-2 and β-arrestin-2 were significantly elevated in cirrhotic patients and rats compared with those of the controls. The interaction of the α 1 adrenergic receptor and β-arrestin-2 was significantly aggravated. This interaction was significantly reversed by GRK-2 inhibitor. Both the protein expression and activity of ROCK-1 were significantly decreased in the mesenteric artery in patients with cirrhosis compared with those of the controls, and this phenomenon was not shown in the cirrhotic rats. Norepinephrine significantly increased the activity of ROCK-1 in normal rats but not in cirrhotic ones. Norepinephrine significantly increased ROCK-1 activity in cirrhotic rats when GRK-2 inhibitor was used. CONCLUSIONS: β-arrestin-2 expression and its interaction with GPCRs are significantly upregulated in the mesenteric arteries in patients and rats with cirrhosis. These upregulations result in GPCR desensitization, G-protein dysfunction and ROCK inhibition. These may explain the decreased contractility of the mesenteric artery in response to vasoconstrictors.

经门静脉注射慢病毒调控目标蛋白表达治疗小鼠肝泡球蚴病方法的建立

经小鼠肝门静脉注射针对EmOPN的慢病毒构建OPN低表达的小鼠肝泡球蚴病治疗模型。将腹腔感染泡球蚴6月的沙鼠剖检,提取泡球蚴原头蚴,肝脏被膜下注射原头蚴法建立C57BL小鼠肝泡球蚴病模型,饲养1月后麻醉下将针对EmOPN的慢病毒Lv-EmOPN-734注射入门静脉,无菌棉按压后电凝穿刺点止血、关腹。普通环境饲养,5 d后随机选取5只小鼠取其肝脏组织,冰冻切片后在激光共聚焦显微镜下观察验证病毒是否进入泡状棘球蚴组织。慢病毒注射2月后对比肝脏及泡球蚴组织生长情况,Western blot检测OPN表达情况。结果门静脉注射慢病毒处理5 d后,慢病毒在正常肝脏组织、囊泡生发层、囊壁、囊外炎细胞层均有分布,其中生发层、囊壁分布较多。Western blot结果表明门静脉注射慢病毒2月后OPN的表达较空白对照组明显降低(P<0.01)。本研究通过门静脉注射慢病毒成功构建低表达OPN的小鼠肝泡球蚴病治疗模型,为通过调控目标蛋白表达治疗小鼠肝泡球蚴病提供建模方法。

光谱法研究天然牛磺酸与肝硬化门静脉高压大鼠的肝组织蛋白相互作用

目的:通过光谱法研究天然牛磺酸(Taurine)与肝硬化门静脉高压大鼠的肝组织蛋白相互作用并探讨其作用机制。方法:将120只大鼠按随机数字法分成正常组、模型组、心得安组、天然牛磺酸组四组,每组30只,除正常组外,其余组用四氯化碳(carbon tetrachloride, CCL4)制备肝硬化门脉高压大鼠模型,造模同时给药。心得安组喂心得安,天然牛磺酸组喂天然牛磺酸,模型组喂等量生理盐水,疗程10周,治疗后对比各组门脉高压数值,并测定不同温度下各组天然牛磺酸药物-大鼠肝组织蛋白体系荧光光谱和天然牛磺酸紫外吸收光谱,根据光谱数据进行分析。结果:天然牛磺酸组大鼠门脉血流量(portal vein flow, PVF)、门脉压力(portal vein pressure, PVP)、门脉阻力(PVR)较心得安组、模型组更低,平均动脉压(mean arterial pressure, MAP)较高。各组大鼠肝组织蛋白的Kq值均大于最大动态猝灭速率2.0×10^(10)L/(mol·s)。大鼠肝组织蛋白体系:焓变(△H):-8 707.633 6;熵变(△S):33.413 95。正常组吉布斯自由能变化(△G)、△H均为负值,△S为正值;天然牛磺酸组△G、△H均为正值,△S为负值,模型组无明显规律。正常组、模型组、天然牛磺酸组R值分别为1.77、2.35、2.28 nm, r值分别为1.24、1.31、6.56。结论:天然牛磺酸具有抗肝纤维化,减轻门脉高压的作用,其机制可能是改变了肝硬化门脉高压大鼠的肝脏组织蛋白结构,从而减轻肝损害。

肝硬化营养不良--从改善门静脉高压获益

肝硬化患者普遍存在营养不良,尤其发展到失代偿期,营养不良发生率高,其表现形式主要为蛋白质-能量营养不良,对患者预后产生负面影响。引起肝硬化营养不良的原因主要为摄入不足和消耗增加。人体成分测定是评估肝硬化营养不良类型的一项重要方法。欧洲肠外与肠内营养学会指南建议所有肝硬化患者均需采用营养风险筛查工具(NRS2002)进行营养风险筛查,评分≥3则存在营养风险。欧洲肠外与肠内营养学会指南推荐肝硬化患者每日能量摄入30~35 kcal/kg,每日蛋白质摄入量为1.2~1.5 g/kg。经颈静脉肝内门体分流术可有效降低肝硬化患者门静脉高压,有助于改善其营养状态。

肝细胞癌临床病理学特征与p53蛋白表达的关系

应用免疫组织化学技术检测29例肝细胞癌（肝癌）和23例肝硬化标本中突变型p53蛋白的表达，并探讨后者与肝癌临床病理学特征之间的关系。结果：肝癌突变型p53蛋白表达阳性率为70％（20／29），癌旁组织阳性率为60％（18／29），肝硬化组织阳性率为30％（7／23），有血管侵犯的12例肝癌变变型p53蛋白表达均为阳性，而无血管侵犯的17例中仅8例为阳性（P＜0．05）；突变型p53蛋白阳性组血清甲胎蛋白（AFP）明显高于阴性组（8370±4764ng／ml比98．7±64．3ng／ml，P＜0．05）。提示：P53蛋白表达在肝硬化时即发生了异常；p53蛋白异常可能是AFP基因被激活的原因之一；p53蛋白异常有利于肝癌向门静脉转移。

血清腹水白蛋白梯度的临床应用价值

目的研究血清腹水白蛋白梯度(SAAG)在腹水性质鉴别中的的临床应用价值。方法选择诊断明确的腹水患者72例,分为门脉高压组40例、非门脉高压组32例,分别测定其血清与腹水中总蛋白和白蛋白的值并进行比较。结果门脉高压组患者SAAG为(19.18±5.22)g/L,非门脉高压组患者SAAG为(7.82±3.12)g/L,两组比较差异有显著性意义(P<0.001)。SAAG对门脉高压诊断的敏感度95%(38/40),特异度96.9%(31/32),准确度95.8%(69/72),阳性预测值97.4%(38/39),阴性预测值93.9%(31/33),均明显高于腹水总蛋白诊断渗、漏出液分类方法。结论血清腹水白蛋白梯度对鉴别门脉高压性腹水和非门脉高压性腹水具有重要的临床价值,值得临床推广应用。

表达HBx的肝前体细胞的小鼠肝内移植模型的构建

目的构建表达乙肝病毒X基因(HBx)的肝前体细胞,并经小鼠门静脉注射建立肝内移植模型,为进一步研究HBx对肝前体细胞的作用和影响及其在原发性肝癌发病机制中的作用奠定了基础。方法分别将表达HBx基因的重组腺病毒Ad-HBx-GFP和空载体Ad-GFP转染小鼠肝前体细胞,再经小鼠门静脉注射后3、7、14 d取血清和肝组织,检测血清丙氨酸氨基转移酶(ALT)变化情况,观察绿色荧光蛋白表达情况,免疫组织化学法观察HBx阳性染色,并取表达高峰在第7天的肝组织,进行Western blot法和实时荧光定量PCR(Real-time PCR)法分别检测HBx的蛋白及mRNA表达。结果成功构建了表达HBx并靶向针对肝前体细胞的小鼠模型,绿色荧光蛋白表达量、免疫组化阳性细胞数量及血清ALT均在注射后第7天达到高峰,RT-PCR及Western blot均检测到第7天14-19/Ad-HBx-GFP组小鼠肝组织目的基因及蛋白的特异性表达,与14-19/Ad-GFP组及生理盐水注射组相比结果具有统计学差异。结论成功构建了表达HBx并靶向针对肝前体细胞的小鼠模型,操作可靠,重复性好,效果稳定,不仅对探讨原发性肝癌的发生机制奠定了基础,也为肿瘤动物模型的构建提供了新的思路。

生长激素对门静脉高压症病人肝蛋白质合成的影响

目的 :了解生长激素 (GH)对经颈静脉肝内门体分流术 (TIPS)后门脉性肝硬化病人肝蛋白质代谢的影响。 方法 :对 1 0例门静脉高压症病人 ,在TIPS术后第 2天开始皮下注射重组人生长激素 (rhGH) 8U× 7天。检测治疗前及治疗后 3、7天血清清蛋白 (Alb)、前清蛋白 (PA)、纤维连接蛋白 (FN)水平 ,同时测定血清胰岛素样生长因子(IGF 1 )水平 ,进行治疗前后的比较。 结果 :血清IGF 1水平TIPS术前与术后比较无显著差异 ,GH治疗后 3天明显升高 (P <0 .0 1 ) ;Alb水平TIPS术前与GH治疗后 3天比较无显著差异 ,7天后明显升高 (P <0 .0 5 ) ;PA和FN水平在GH治疗后第 3天开始升高 ,第 7天明显升高 (P <0 .0 1 )。 结论

门静脉高压病人不同术式对肝蛋白质合成及储备功能的影响

目的 :探讨门静脉高压病人不同术式对肝蛋白质合成与储备功能的影响。 方法 :对门静脉高压病人分别实施断流术 (Hassab1 6例 )、分流术 (脾 肾静脉分流 1 0例 ,肠系膜上静脉 下腔静脉分流 2例 )、联合手术 (Hassab +脾 肾静脉分流 8例 ) ,检测其术前、术后 6个月、2 4个月血糖、清蛋白、前清蛋白、转铁蛋白、胰岛素、高血糖素的变化。 结果 :肝硬化门静脉高压病人清蛋白、前清蛋白、转铁蛋白均比对照组低 (P <0 .0 5 )。不同术式、不同时期蛋白质合成 (尤其前清蛋白 )改善显著 ,门静脉高压手术前、后均低于对照组 (P <0 .0 5 ) ;断流术组清蛋白、转铁蛋白术后2 4个月明显好于其他各组 ,联合手术组与断流术组接近 ,高于分流术组 (P <0 .0 5 )。断流术组和联合手术组 6个月后空腹血糖获得明显改善 ,胰岛素、高血糖素及二者比值均升高 ,且高于对照组和门静脉高压术前组 (P <0 .0 5 )。联合手术组胰岛素、高血糖素的水平则有下降趋势 (P <0 .0 5 )。 结论 :联合手术较断流和分流手术对肝蛋白质合成和储备功能影响较小。

蛋白激酶Cα在门脉高压患者肝内外血管的表达

对 34例门脉高压患者的肝内外血管与 30例对照组织行 HE染色观察形态学变化 ;行蛋白激酶 Cα (PKCα)免疫组化染色并行定量分析。结果发现门脉高压患者肝外血管呈门脉高压性血管病变 ,肝内有微循环障碍。正常肝内外血管 PKCα免疫组化染色呈阴性或弱阳性 ,门脉高压患者的肝脏和脾动静脉呈强阳性 ,定量分析二者差异有显著性 (P<0 .0 1)。提示 :PKCα过度表达可能是门脉高压肝内外血管结构改变的重要原因 ,并可能改变其血管舒缩活性物质的合成及敏感性。

TpP、D-D联合监测对门静脉血栓形成的早期预测价值

目的探讨联合监测血栓前体蛋白(TpP)、D-二聚体(D-D)在早期预测门静脉高压症患者术后门静脉血栓(PVT)形成中的价值。方法选取因门静脉高压行脾脏切除(或联合血管断流)术的48例患者,将术后PVT形成的26例患者作为观察组,术后无PVT形成的22例患者作为对照组。对两组患者术前1d及术后第1、3、5、7、14天TpP、D-D的水平进行比较分析。结果两组患者术前TpP及D-D水平并无明显差异(均P>0.05),而观察组术后第1、3、5、7天TpP及D-D水平均明显高于对照组,差异均有统计学意义(均P<0.05)。不同手术方式患者术后第1天TpP及D-D水平比较差异均无统计学意义(均P>0.05)。术后第1天D-D检测的灵敏度达84.6%,诊断符合率为81.3%,误诊率为22.7%;TpP检测的灵敏度高达88.5%,诊断符合率为75.0%,误诊率为40 9%。D-D的曲线下面积(AUC)为0.891,TpP为0.875;两者联合,其AUC可达0.912。结论 TpP、D-D两者联合检测有助于PVT的早期预测。

新生儿腹部超声门静脉积气征阳性的病例对照研究

背景对于有血便、腹胀等表现且腹部超声门静脉积气征(PVG)阳性的新生儿,临床上仍存在将食物蛋白过敏性直肠结肠炎(FPIPC)误诊为NEC的情况。目的比较NEC和FPIPC的临床资料及腹部超声表现,并分析NEC的相关因素。设计病例对照研究。方法纳入2019年1月1日至12月31日在重庆医科大学附属儿童医院住院、至少1次腹部超声检查显示PVG阳性的新生儿,根据出院时第一诊断分为NEC组和FPIPC组。从电子病历中截取患儿的一般资料、临床表现和体征、实验室检查结果、腹部超声报告等,行影响因素分析。主要结局指标腹部超声检查PVG阳性的新生儿中确诊为NEC的影响因素。结果NEC组68例,FPIPC组42例。NEC组胎龄、入院日龄小于FPIPC组,出生体重和入院体重低于FPIPC组,腹胀、反应低下、肠鸣音减弱的百分比高于FPIPC组,N%高于FPIPC组,CRP升高和PCT异常的百分比高于FPIPC组;FPIPC组腹泻的百分比高于NEC组;差异均有统计学意义。腹部超声检查:NEC组肠蠕动减慢、腹腔积液的比例高于FPIPC组,差异均有统计学意义;PVG阳性检出日龄在两组间差异无统计学意义;腹部超声复查(NEC组67例,FPIPC组37例)3 d内PVG未消失的比例在两组间差异无统计学意义。Logistic回归发现,腹部肠鸣音减弱(OR=14.7,95%CI:2.6~82.2,P=0.002)、CRP>10 mg·L^(-1)(OR=24.7,95%CI:1.4~431.7,P=0.028)、超声示肠蠕动减慢(OR=26.9,95%CI:1.8~389.9,P=0.016)与NEC相关。结论新生儿腹部超声PVG阳性时,需结合胎龄、出生体重、临床表现、炎症指标、腹部超声特点等进行鉴别诊断,当腹部肠鸣音减弱、CRP增高、腹部超声示肠蠕动减慢时,需警惕NEC。

P-sel、TpP、D-D联合检测预测门静脉高压症患者术后发生门静脉血栓的价值

目的探讨P-选择素(P-sel)、血栓前体蛋白(Tp P)和D-二聚体(D-D)联合检测预测门静脉高压症患者术后并发门静脉血栓的价值。方法选择2010年8月至2013年9月于我院行门静脉高压症手术的68例患者作为研究对象,患者分别于手术前后进行P-sel、Tp P和D-D的含量检测,根据术后血栓发生与否进行分组,并对检测结果进行比较分析。结果患者术后发生血栓37例(血栓组),未发生血栓31例(正常组),术后1 d血栓组患者P-sel、Tp P及D-D浓度均较术前明显升高,术后7 d逐渐降低,而正常组患者术后14 d内均无明显变化,差异具有统计学意义(P<0.05)。三项指标检测在术后第一天预测门静脉血栓形成方面特异性最高者为P-sel,其次为D-D、Tp P,灵敏度表现为Tp P>D-D>P-sel的特点,且P-sel的误诊率最低,仅为8.8%。结论术后并发门静脉血栓患者大多术后第一天即可出现P-sel、Tp P和D-D浓度显著升高,而术后P-sel、Tp P和D-D三项的检测结果对预测门静脉血栓的形成具有辅助作用。

奥曲肽联合普萘洛尔治疗肝硬化上消化道出血患者效果及对炎性指标水平和门、脾静脉血流影响

目的观察奥曲肽联合普萘洛尔治疗肝硬化上消化道出血患者的效果及对炎性指标水平和门、脾静脉血流的影响。方法选取肝硬化上消化道出血78例,根据治疗方法不同将其分为奥曲肽联合普萘洛尔组(43例)和奥曲肽组(35例)两组。奥曲肽联合普萘洛尔组采用醋酸奥曲肽联合盐酸普萘洛尔治疗,奥曲肽组仅采用醋酸奥曲肽治疗。观察比较两组治疗3 d后临床效果,治疗前及治疗3 d后血清炎性指标水平及门静脉血流量(PVF)、脾静脉血流量(SVF),以及治疗期间不良反应发生情况。结果治疗3 d后,奥曲肽联合普萘洛尔组总有效率高于奥曲肽组,差异有统计学意义(P<0.05)。治疗前,两组血清炎性指标水平及PVF、SVF比较差异均无统计学意义(P>0.05)。治疗3 d后,两组血清C反应蛋白(CRP)、白细胞介素6(IL-6)水平及PVF、SVF均较治疗前降低,血清白细胞介素10(IL-10)水平均较治疗前升高;且奥曲肽联合普萘洛尔组血清CRP、IL-6水平及PVF、SVF低于奥曲肽组,血清IL-10水平高于奥曲肽组,差异有统计学意义(P<0.01)。治疗期间,两组不良反应总发生率比较差异无统计学意义(P>0.05)。结论奥曲肽联合普萘洛尔治疗肝硬化上消化道出血患者可提高临床效果,减轻炎症反应,改善门、脾静脉血流情况,且安全性良好。

肝门部胆管癌细胞系FRH 0201与正常肝细胞系L02蛋白质组学差异分析

目的:分析肝门部胆管癌细胞系FRH0201与正常肝细胞系L02的蛋白质表达差异,筛选肝门部胆管癌的潜在分子标志物。方法:应用表面增强激光解吸离子化(surface enhanced laser desorption/ionization,SELDI)蛋白质芯片技术检测肝门部胆管癌及正常肝细胞系的蛋白质谱。用PBSII-C型蛋白质芯片阅读机读取数据,采用Proteinchip软件分析数据。结果:IMAC3、WCX2两种蛋白芯片共捕获144个蛋白峰,发现16个差异蛋白。与正常肝细胞系L02蛋白谱相比,4个蛋白在肝门部胆管癌细胞系FRH0201中高表达,12个蛋白在肝门部胆管癌细胞系FRH0201中低表达。结论:肝门部胆管癌与正常肝细胞存在差异蛋白表达,这些差异蛋白有可能成为潜在的肝门部胆管癌标志物,对其进行研究有助于了解肝门部胆管癌的发病机制。