慢性胃炎患者胃黏膜三叶因子1与细胞间黏附分子1蛋白表达

[目的]在幽门螺杆菌(Hp)阴性慢性浅表性胃炎(CSG)中探讨脾胃湿热证与三叶因子1(TFF1)、细胞间黏附分子1(ICAM-1)蛋白表达的相关性。[方法]Hp阴性CSG患者(脾胃湿热组27例,脾虚组10例)及对照组10例,经临床检查、胃镜取标本、病理学及免疫组化SP法检测胃黏膜炎症程度及TFF1、ICAM-1的蛋白表达情况。[结果]胃镜下脾胃湿热组胃黏膜充血水肿较脾虚证明显。炎症程度:脾胃湿热组>对照组(P<0.01),脾虚组>对照组(P<0.05),脾胃湿热组稍重于脾虚组。TFF1蛋白表达:脾胃湿热组>脾虚组>对照组。ICAM-1蛋白表达:脾胃湿热组>脾虚组稍高于对照组。ICAM-1蛋白表达与炎症程度呈正相关(P<0.01)。TFF1与ICAM-1蛋白表达呈正相关(P<0.01)。[结论]脾胃湿热证时TFF1、ICAM-1蛋白均呈高表达。提示脾胃湿热证中TFF1可能与机体正气抗邪状态有关;ICAM-1可能参与湿邪致病的分子机制。     

慢性浅表性胃炎脾胃湿热证与热休克蛋白7O表达的关系

[目的]探讨慢性浅表性胃炎（CSG）脾胃湿热证与热休克蛋白70（HSP70）表达的关系。[方法]睽沿患者38例,其中脾胃湿热证22例、脾气虚证16例,另10例正常人为对照。胃镜下取胃窦黏膜,采用免疫组织化学检测HSP70蛋白表达情况。[结果]脾胃湿热证组和脾虚证组HSP70蛋白表达明显高于正常对照组（P〈0．01）}脾胃湿热证组各亚型中,HSP70表达水平呈热重于湿〉湿热并重〉湿重于热的趋势。[结论]HSP70属于人体“阳气”范畴,HSP70以热证表达最为明显,具有证的特异性;“热”与“湿”在脾胃湿热证中的比分会影响HSPT0在脾胃湿热证型中的表达：热邪提高HSP70表达,湿邪抑制HSP70表达。     

隆起糜烂性胃炎证型与幽门螺杆菌感染及热休克蛋白60和70表达的相关性

[目的]探讨隆起糜烂性胃炎(Raised Erosive Gastritis,REG)中医证型与幽门螺杆菌(Hp)感染和病理组织学及热休克蛋白60(HSP60)、热休克蛋白70(HSP70)表达的关系,以期指导中西医结合防治REG。[方法]选择131例REG患者按中医辨证分为脾胃湿热证32例(Hp阳性19例,阴性13例),脾胃气虚证52例(Hp阳性者34例,阴性18例),脾虚湿热证47例(Hp阳性者33例,阴性14例)。所有受试者均行胃镜检查,取胃窦部活检标本行快速尿素酶试验及组织染色法检测Hp;病理组织学检查及免疫组织化学检测HSP60,其中63例免疫组织化学检测HSP70。并设正常对照(正常)组18例。[结果]REG脾虚湿热证组的萎缩、肠化生(IM)程度均高于脾胃湿热证及脾胃气虚证组(P0.05),而后2组之间比较以及3组中Hp阳性者与阴性者比较差异均无统计学意义(P0.05)。3组HSP60表达均较正常组增加(P0.01),而3组之间比较均P0.05;脾胃湿热证及脾虚湿热证组中Hp阳性者的HSP60表达均高于Hp阴性者(P0.05),而脾胃气虚组中的Hp阳性与Hp阴性者比较P0.05。3组的HSP70表达均较正常组增加(P0.01);而3组的HSP70阳性表达情况分别比较均P0.05;脾胃湿热证组中Hp阴性的HSP70表达高于Hp阳性者(P0.05),而脾胃气虚证组与脾虚湿热证组中Hp阳性者与阴性者HSP70表达比较均P0.05。REG Hp阳性者胃黏膜HSP60的表达明显高于Hp阴性(P0.01);REG Hp阳性者胃黏膜HSP70的表达与Hp阴性者比较P0.05。[结论]REG脾虚湿热证患者胃黏膜萎缩、IM程度均高于脾胃气虚证及脾胃湿热证。REG3组胃黏膜HSP60及HSP70的表达均较正常组增强。Hp感染可诱导胃黏膜HSP60的高表达。HSP60表达既与Hp感染有关,又与湿热之邪有关。     

慢性胃炎脾气虚证患者胃窦黏膜内表皮生长因子和三叶因子表达的意义

[目的] 探讨慢性胃炎脾气虚证患者胃窦黏膜内表皮生长因子(EGF)和三叶因子(TFF1)表达的意义。[方法] 采用免疫细胞化学染色的方法。检测慢性胃炎脾气虚和脾胃湿热患者及胃窦黏膜内EGF和TFF1 的表达,并与正常对照者比较。[结果] 脾气虚组和脾胃湿热组患者EGF和TFF1 的表达与正常对照组比较差异有显著性意义(P<0 .05,P<0. 01)。两组间EGF比较差异也有统计学意义(P<0. 01),在两组间TFF1(++)比较差异无统计学意义,但脾气虚组TFF1的阳性率高于脾胃湿热组。脾胃湿热组Hp的感染率高于脾气虚组(P<0 .01)。[结论] 脾气虚组EGF的表达高于脾胃湿热组,可能与后者Hp感染率较高有关;脾气虚组TFF1的表达高于脾胃湿热组,可能与胃黏膜严重损伤有关。     

三叶因子1与慢性浅表性胃炎脾胃湿热证研究进展

三叶因子1(trefoil factor 1,TFF1)又名乳癌相关肽(breast cancer associated peptide,即pS2),是TFF家族成员之一,目前哺乳动物体内发现的还有TFF 2和TFF 3[1]。TFF是一群主要由胃肠道黏液细胞分泌的小分子多肽,在胃肠黏膜保护与损伤修复,促进黏膜重建等方面发挥重要作用。因TFF1主要分布于胃黏膜,在胃黏膜保护及修护方面有重要作用,故已被广泛用于胃肠黏膜炎症、癌前病变及胃肠肿瘤等领域的研究。当前脾胃湿热证炎症机制方面的研究已取得较大进展,现就保护因子TFF1与慢性浅表性胃炎(CSG)脾胃湿热证研究的进展综述如下。1 TFF1…     

慢性浅表性胃炎胃黏膜增殖细胞核抗原和热休克蛋白与中医证型的关系

[目的]研究慢性浅表性胃炎（CSG）胃黏膜增殖细胞核抗原（Proliferating cell nuclear antigen,PCNA）和热休克蛋白60（Heat shock protein 60,HSP60）的表达与中医证型的关系。[方法]免疫细胞化学技术检测CSG患者不同证型胃窦黏膜内PCNA和HSP60的水平。[结果]CSG脾气虚证PCNA胃黏膜内的细胞分裂指数高于脾胃湿热证（P〈0．05）;脾胃湿热证胃黏膜内的HSP60在间质和腺体均高于脾气虚证（P〈0．05,〈0．01）,而2种证型HSP60在胃黏膜上皮的表达比较差异无统计学意义（P〉0．05）。[结论]中医的临床辨证分型与PCNA和HSP60表达有一定关系。     

隆起糜烂性胃炎证型与幽门螺杆菌感染及p53和增殖细胞核抗原表达的相关性

[目的]通过观察隆起糜烂性胃炎(Raised Erosive Gastritis,REG)中医证型与幽门螺杆菌(Hp)感染和p53、增殖细胞核抗原(PCNA)表达之间的关系,以期更好的协助指导中西医结合防治REG。[方法]选择REG中医辨证符合脾胃湿热证、脾胃气虚证、脾虚湿热证的患者63例,并设正常对照(正常)组18例,所有受试者均行胃镜检查,取胃窦部活检标本行快速尿素酶试验及组织染色法检测Hp及p53、PCNA。[结果]REG组各证型的p53、PCNA表达均较正常组增加(均P0.01);各证型的p53、PCNA阳性表达分别比较差异均无统计学意义(均P0.05);各证型Hp阳性与Hp阴性者p53、PCNA阳性表达比较差异均无统计学意义(均P0.05)。[结论]REG胃黏膜处于高增殖状态。REG中医各证型间与Hp感染及p53、PCNA表达无明显差异。     

“湿”证与幽门螺旋杆菌感染的相关性及对胃黏液蛋白MUCA5AC、MUC6、MUC1表达的影响

[目的]探索"湿"证与幽门螺旋杆菌(HP)感染的相关性及对胃黏膜屏障中胃黏液蛋白MUCA5AC、MUC6、MUC1表达的影响。[方法]以随机数字表法将研究对象分为观察组(湿证)和对照组(健康体检人群),每组各80例,研究与HP感染的相关性,并进一步探索2组胃黏膜中MUCA5AC、MUC6、MUC1因子的表达情况。[结果]湿证组中HP阳性率明显高于对照组,2组之间差异有统计学意义(P<0.05)。湿证与HP感染呈正相关(r=0.681,P<0.01)。观察组胃黏膜中MUCA5AC、MUC6、MUC1因子表达明显低于对照组(P<0.05)。[结论]湿邪能降低胃黏膜屏障中黏液蛋白的表达,破坏胃黏膜屏障,可能是HP感染或复发的关键病理因素。     

脾胃湿热证胃病患者胃黏膜细胞凋亡基因相关蛋白的表达

[目的]探讨脾胃湿热证胃病患者胃黏膜细胞凋亡基因相关蛋白的表达。[方法]选取脾胃湿热证胃病患者70例,检测胃黏膜Fas、p53、增殖细胞核抗原(PCNA)、Bcl-2凋亡基因相关蛋白。并与70例脾胃虚寒证胃病患者进行对照。[结果]脾胃湿热证以糜烂性胃炎多见(58.6%),而脾胃虚寒证以萎缩性胃炎多见(22.9%)。脾胃湿热证患者Fas、p53表达明显高于脾胃虚寒证患者,阳性率分别为74.3%、75.7%和55.7%、64.3%(P<0.05),而PCNA、Bcl-2表达则与脾胃虚寒证患者差异无统计学意义。[结论]脾胃湿热证胃病患者胃黏膜细胞有促凋亡基因相关蛋白的过度表达。     

黏蛋白和肠三叶因子在溃疡性结肠炎中的表达

[目的]研究溃疡性结肠炎(UC)结肠黏膜中的黏蛋白MUC2、MUC5AC以及肠三叶因子(TFF3)的表达规律及其与中医证型的关系。[方法]选择UC患者74例,其中大肠湿热证组48例,脾胃气虚证组26例,另外选10例健康体检人群为正常对照组。通过免疫组织化学染色法测定3组人群肠黏膜上皮中MUC2、MUC5AC以及TFF3的表达情况。[结果]MUC2在UC大肠湿热组、脾胃气虚组患者表达较正常对照组减少,但差异无统计学意义(P0.05)。大肠湿热组、脾胃气虚组MUC5AC的阳性表达率分别为33.3%和23.1%,正常对照组均为阴性,大肠湿热组MUC5AC阳性表达率与正常对照组相比差异有统计学意义(P0.05),而脾胃气虚组与正常对照组对比差异无统计学意义。大肠湿热组TFF3阳性表达率为79.2%,高于脾胃气虚组的53.9%,两者的阳性表达与正常对照组相比,均差异有统计学意义(P0.05)。脾胃气虚组与大肠湿热组间MUC2、MUC5AC以及TFF3的表达均差异无统计学意义(P0.05)。[结论]UC大肠湿热证MUC5AC的表达上调和TFF3的表达下调可能与UC的发生、发展有关,而且对临床诊疗、判断预后也有较大意义。     

Cytochrome 1A1 and 1B1 gene diversity in the Zanzibar islands

Amodiaquine (AQ) is a 4‐aminoquinoline widely used in the treatment of malaria as part of the artemisinin combination therapy (ACT). AQ is metabolised towards its main metabolite desethylamodiaquine mainly by cytochrome P450 2C8 (CYP2C8). CYP1A1 and CYP1B1 play a minor role in the metabolism but they seem to be significantly involved in the formation of the short‐lived quinine‐imine. To complete the genetic variation picture of the main genes involved in AQ metabolism in the Zanzibar population, previously characterised for CYP2C8, we analysed in this study CYP1A1 and CYP1B1 main genetic polymorphisms. The results obtained show a low frequency of the CYP1A1*2B/C allele (2.4%) and a high frequency of CYP1B1*6 (approximately 42%) followed by CYP1B1*2 (approximately 27%) in Zanzibar islands. Genotype data for CYP1A1 and CYP1B1 show a low incidence of fast metabolisers, revealing a relatively safe genetic background in Zanzibar’s population regarding the appearance of adverse effects.     

Polymorphisms of the glutathione S-transferases mu-1 (GSTM1) and theta-1 (GSTT1) and the risk of advanced alcoholic liver disease

OBJECTIVE: The aim of this study was to determine whether null genotypes for glutathione transferase mu-1 (GSTM1) and theta-1 (GSTT1) influence the risk of development of advanced alcoholic liver disease. MATERIAL AND METHODS: GSTM1 and GSTT1 genotypes were identified on DNA through multiple analysis with polymerase chain reaction in 153 subjects diagnosed with advanced alcoholic liver disease and in 241 healthy controls. RESULTS: The frequency of the GSTM1 null genotype was not different between patients and controls (36.6% versus 41.1%, non-significant). The GSTT1 null genotype was more frequently found in patients than in controls (32% versus 22%, odds ratio 1.67, 95% CI 1.03-2.71, p =0.027). Moreover, patients were more likely to be simultaneous carriers of both GSTM1 and GSTT1 null genotypes (odds ratio 4.30, 95% CI 1.89-9.97, p =0.0003). CONCLUSIONS: The GSTT1 null genotype is more frequent among patients with advanced alcoholic liver disease than in controls. The coincidence of this genotype with the GSTM1 null genotype is four times more likely in patients. We suggest that polymorphisms affecting the activity of the glutathione S-transferase isoforms M1 and T1 may be associated with the risk of developing chronic severe ethanol liver damage.     

Polymorphisms of the glutathione S-transferases mu-1 (GSTM1) and theta-1 (GSTT1) and the risk of advanced alcoholic liver disease

Objective. The aim of this study was to determine whether null genotypes for glutathione transferase mu-1 (GSTM1) and theta-1 (GSTT1) influence the risk of development of advanced alcoholic liver disease. Material and methods. GSTM1 and GSTT1 genotypes were identified on DNA through multiple analysis with polymerase chain reaction in 153 subjects diagnosed with advanced alcoholic liver disease and in 241 healthy controls. Results. The frequency of the GSTM1 null genotype was not different between patients and controls (36.6% versus 41.1%, non-significant). The GSTT1 null genotype was more frequently found in patients than in controls (32% versus 22%, odds ratio 1.67, 95% CI 1.03–2.71, p=0.027). Moreover, patients were more likely to be simultaneous carriers of both GSTM1 and GSTT1 null genotypes (odds ratio 4.30, 95% CI 1.89–9.97, p=0.0003). Conclusions. The GSTT1 null genotype is more frequent among patients with advanced alcoholic liver disease than in controls. The coincidence of this genotype with the GSTM1 null genotype is four times more likely in patients. We suggest that polymorphisms affecting the activity of the glutathione S-transferase isoforms M1 and T1 may be associated with the risk of developing chronic severe ethanol liver damage.     

糖尿病肾病与MCP-1、SICAM-1的相关性及辛伐他汀对其干预治疗的作用

目的 探讨糖尿病肾病(DN)与血清单核细胞趋化蛋白1(MCP-1)、可溶性细胞问黏附分子1(sI-CAM-1)的相关性,以及辛伐他汀干预治疗对早期DN的作用.方法将60例DN患者随机分为对照组和辛伐他汀治疗组,治疗16周后,观察两组血清MCP-1、sICAM-1及尿白蛋白排泄率(UAER)变化,评价辛伐他汀对患者肾脏的保护作用.结果 与对照组比较,治疗组血清MCP-1、sICAM-1及UAER均明显降低(P均<0.05).结论 辛伐他汀对早期DN患者有肾脏保护作用,能延缓其进展为终末期肾病.     

血管生成素1和血栓调节蛋白1在STZ鼠肾脏中的表达及其意义

目的：探讨血管生成素1（angiopoietin-1,Ang-1）和血栓调节蛋白1（thrombomodulin-1,TM-1）在糖尿病鼠肾脏中的表达变化及其与肾脏微血管病变的关系. 方法：STZ诱导的糖尿病大鼠肾病模型,设正常对照和模型组,于2、4、8、12、16、20、24周,采用免疫组化观察肾脏Ang-1和TM-1表达变化以及RT-PCR观察肾脏Ang-1mRNA表达,并行相关性分析. 结果：糖尿病组4和8周时肾脏Ang-1mRNA表达显著上调, 24周时明显低于对照组;糖尿病组4～24周免疫组化显示肾小球Ang-1着染均显著高于对照组,峰值在4～8周,12周后逐渐下调;糖尿病组2～20周肾小球TM-1明显增强;Ang-1和TM-1呈正相关. 结论：糖尿病肾脏存在Ang-1和TM-1的异常改变,表现为早中期表达上调,后期表达下调,并且这种改变可能与糖尿病肾脏新生血管的生成有关.     

Concerning the significance of paraoxonase-1 and SR-B1 genes in atherosclerosis

High-density lipoprotein (HDL) is an independent protective factor against cardiovascular disease. The enzyme paraoxonase-1 (PON-1) contributes to the anti-atherogenic effects of HDL. In vitro studies have demonstrated that paraoxonase's substrates are highly heterogeneous and that some contribute to the development of atherosclerotic lesions. The atheroprotective role of PON-1 was established in genetically engineered animal models. In humans, the PON-1 Gln192Arg and Met55Leu polymorphisms appear to be associated with increased susceptibility to cardiovascular disease and with different PON-1 activity levels and concentrations. The CLA-1 (CD36 and Lysosomal integral membrane protein-II Analogous-1) gene is the human homologue of the murine SR-B1 (Scavenger Receptor class B type 1) gene. SR-B1 was the first high-affinity HDL receptor to be identified at the molecular level. The CLA-1 receptor plays a pivotal role in HDL-mediated reverse cholesterol transport by mediating the selective uptake of free cholesterol as well as of native and oxidized cholesteryl esters. Its atheroprotective role has also been established in transgenic mice studies. Several polymorphic variants of the CLA-1 gene have been described, some of which are associated with phenotypic changes in plasma lipoproteins. Both genes participate in the complex HDL metabolic pathway and, presumably, also in defense mechanisms against oxidative stress.