PPAR-γ和survivin基因表达与直肠癌进展的关系

目的探讨过氧化物酶体增殖因子活化受体(PPAR)-γ和存活素(survivin)基因表达与直肠癌进展的关系。方法选取该院自2011年5月至2015年5月临床以及病理资料均齐全并经手术切除方式获得的直肠癌患者大体石蜡标本85例,取同期手术切除的腺瘤组织82例以及同期接受痔上黏膜环切手术治疗后的良性病变组织80例。采用免疫组织化学法分析PPAR-γ及survivin蛋白表达,分析其与患者病理特征的关系,采用Logistic回归分析PPAR-γ及survivin蛋白表达的相关因素。结果癌组织的PPAR-γ及survivin蛋白表达的阳性率明显高于正常组织及腺瘤组织(P<0.05)。正常组织与腺瘤组织PPAR-γ及survivin蛋白表达的阳性率比较差异无统计学意义(P>0.05)。直肠癌患者PPAR-γ及survivin蛋白表达与病理情况的分化程度、淋巴结转移及Dukes分级有关,而与年龄及性别无关。Logistic回归分析法显示,影响直肠癌患者PPAR-γ及survivin蛋白表达的相关因素有低分化、有淋巴结转移以及Dukes分级为C~D级。结论 PPAR-γ和survivin在直肠癌患者组织中高表达,与直肠癌患者的疾病进展有较大关联。     

用蛋白质芯片技术检测结直肠癌患者的肿瘤标志物

肿瘤标志物的检测有助于恶性肿瘤的早期诊断和监测 ,同时检测多种标志物可以提高敏感性。蛋白质芯片是一种高质量、高灵敏度、高特异性且微型化的蛋白质分析技术[1,2 ] 。本实验采用肿瘤诊断用蛋白芯片试剂盒 ,对结直肠癌患者血清中的肿瘤标志物ＣＥＡ ,ＣＡ19 9,ＣＡ2 4 2进行联合检测。一、材料和方法1.标本取自 :①结直肠癌组 :30例经临床病理确诊但未经治疗的结直肠癌患者 ;②正常对照组 :15 9例年龄小于 30岁的健康体检者 ,2 0 6例年龄在 30～ 6 0岁的健康体检者 ,92例年龄大于 6 0岁的健康体检者 ;③疾病对照组 :炎症 89例、良性肿瘤 …     

PPARγ与消化道肿瘤关系的研究进展

过氧化物酶体增殖物激活受体(PPARs)是甾体激素受体超家族的新成员，共有3个亚型(α、β、γ)，是一类核转录因子。PPARγ主要表达在脂肪组织及免疫系统，在结肠、视网膜中也有一定程度表达。近来研究显示，PPARγ与消化道肿瘤的发生有关。PPARγ被其配体激活，可诱导其下游的靶基因表达上调或下调，调控细胞的增殖、分化与凋亡，从而影响肿瘤细胞的形成、生长与转移。     

PPARγ及其配体与肝纤维化的研究进展

慢性肝病疾患是一类世界性的严重危害人们健康的主要疾病,其中肝纤维化(hepatic fibrosis,HF)是这个过程的中间及关键环节.肝星状细胞(hepatic stellate caell,HSC)时启动整个事件的开端,在HF过程中扮演着重要的角色.在进展期的HF中,活化HSC在肝损伤部位移行、增殖,表达各种细胞外基质(extreacellular matrix,ECM)成分和细胞因子,是HF形成的中心环节.     

过氧化物酶体增殖物活化受体与乙型肝炎病毒的复制及肝纤维化的关系

过氧化物酶体增殖物激活受体(peroxisome proliferator activated receptor，PPAR)是一种由配体激活的核转录因子。近年研究发现。PPAR能够调节炎症反应、控制细胞周期和细胞凋亡，其中也包括一些肝炎相关疾病，如乙型肝炎病毒(HBV)的复制、肝纤维化以及肝癌等。本文主要论述。PPAR与HBV复制、肝纤维化的关系。     

组蛋白去乙酰化酶抑制剂及PPARγ激动剂在甲状腺肿瘤治疗中的作用

手术、放射性碘及促甲状腺激素抑制治疗等常规疗法对低分化及未分化甲状腺肿瘤疗效不佳。组蛋白去乙酰化酶（HDAC）作为调控基因转录的关键蛋白酶,其功能异常与肿瘤的发生、发展密切相关。过氧化物酶体增殖物活化受体（PPAR）γ属于激素核受体超家族之一,与细胞的生长、分化密切相关。近来发现HDAC抑制剂及PPARγ激动剂可通过抑制肿瘤细胞增殖、促进其凋亡、诱导其再分化治疗血液系统肿瘤及包括甲状腺肿瘤在内的多种实体瘤,为低分化及未分化甲状腺肿瘤的治疗提供了新思路。     

过氧化物酶体增殖物激活受体α、γ配体对泡沫细胞胆固醇流出及相关基因表达影响的实验研究

目的 观察过氧化物酶体增殖物激活受体（PPAR）α、γ配体对泡沫细胞内胆固醇酯、OX-LDL和三磷酸腺苷结合盒转运体A1（ABCA1）、小凹蛋白-1（caveolin-1）表达的影响。方法 用TBARS法检测细胞内MDA。用油红O染色法检测泡沫细胞的形成。用荧光分光光度法检测细胞内总胆固醇、游离胆固醇和胆固醇酯含量。ELISA法检测泡沫细胞内OX-LDL。用RT-PCR和Western blot检测ABCA1、caveolin-1 mRNA与蛋白的表达。结果 单核细胞经佛波醇酯和OX-LDL孵育后,有大量泡沫细胞形成,细胞内积聚的总胆固醇、游离胆固醇、胆固醇酯及脂质过氧化产物、OX．LDL均明显增多（P〈0．05）,而ABCA1、caveolin-1蛋白、mRNA水平明显减少（P〈0．05）,PPARα、γ配体干预组显著缓解上述变化,细胞内胆固醇酯显著减少,ABCA1、caveolin-1 mRNA和蛋白表达明显增加（P〈0．05）。结论PPARα、γ配体可能通过增强ABCA1、caveolin-1的表达和降低细胞内胆固醇聚积发挥抗动脉粥样硬化的作用。     

过氧化物酶体增殖物激活受体γ配体对诱导大鼠肝癌的抑制作用

过氧化物酶体增殖物激活受体γ(peroxisome pronferatorsactivated receptor gamma，PPARγ)是一种核受体，与基因转录调节及脂类代谢有关。有研究报告PPARγ配体处理癌细胞后可以引起细胞分化和凋亡，提示其可能是一种化学防癌剂而具有潜在应用价值。本研究使用3种PPARγ配体，以了解PPARγ在大鼠肝癌模型中的防癌作用。     

过氧化物酶体增殖物激活受体γ基因转染对小鼠骨髓基质细胞向心肌细胞分化影响的研究

目的 探讨过氧化物酶体增殖物激活受体γ(peroxisome proliferator-activated receptor γ,PPAR γ)基因表达对骨髓基质细胞(marrow stroma cell,MSC)向心肌细胞分化的影响及其调控作用。方法 原代培养Balb/c纯系小鼠MSC,应用脂质体转染法将pEGFP-N1-PPARγ表达载体转入MSC中,CA18筛选。RT-PCR检测mRNA表达,Western blot法检测蛋白表达。结果 未分化的MSC中PPARγmRNA不表达,GATA4、MEF2C、Nkx2.5表达呈阳性。经pEGFP-N1-PPARγ2转染后,调控成心肌细胞方向分化的转录因子GATA4(0.172±0.034对0.053±0.022,P<0.01)、MEF2C(0.164±0.041对0)、Nkx2.5(0.156±0.029对0)mRNA表达明显下调。MSC向成脂肪细胞方向分化,而向成心肌细胞分化受阻。结论 PPARγ抑制MSC分化过程中GATA4、MEF2C、Nkx2.5 mRNA的表达,抑制MSC向成心肌细胞分化,并促进其向脂肪细胞分化。     

噻唑烷二酮类药物对骨骼的影响

In women,short-term clinical trials demonstrated substantial bone loss with thiazolidinedi-one. Pioglitazone and rosiglitazone are widely used to treat diabetes, and better knowledge of their skeletal effects is crucial to guide clinical decisions. The randomized trial provides that rosiglitazone causes bone loss. An imbalance in fracture rates was identified in a final review of adverse event reports in ADOPT trial. That may result from the loss of bone mass due to thiazolidinedione. Animal and in vitro studies suggest that activ-tion of PPARγ promotes adipegenesis at the expense of osteoblastogenesis, and therefore inhibit bone forma-tion and induce bone loss.     

噻唑烷二酮类药物对骨骼的影响

In women,short-term clinical trials demonstrated substantial bone loss with thiazolidinedi-one. Pioglitazone and rosiglitazone are widely used to treat diabetes, and better knowledge of their skeletal effects is crucial to guide clinical decisions. The randomized trial provides that rosiglitazone causes bone loss. An imbalance in fracture rates was identified in a final review of adverse event reports in ADOPT trial. That may result from the loss of bone mass due to thiazolidinedione. Animal and in vitro studies suggest that activ-tion of PPARγ promotes adipegenesis at the expense of osteoblastogenesis, and therefore inhibit bone forma-tion and induce bone loss.     

噻唑烷二酮类药物对骨骼的影响

In women,short-term clinical trials demonstrated substantial bone loss with thiazolidinedi-one. Pioglitazone and rosiglitazone are widely used to treat diabetes, and better knowledge of their skeletal effects is crucial to guide clinical decisions. The randomized trial provides that rosiglitazone causes bone loss. An imbalance in fracture rates was identified in a final review of adverse event reports in ADOPT trial. That may result from the loss of bone mass due to thiazolidinedione. Animal and in vitro studies suggest that activ-tion of PPARγ promotes adipegenesis at the expense of osteoblastogenesis, and therefore inhibit bone forma-tion and induce bone loss.     

噻唑烷二酮类药物对骨骼的影响

In women,short-term clinical trials demonstrated substantial bone loss with thiazolidinedi-one. Pioglitazone and rosiglitazone are widely used to treat diabetes, and better knowledge of their skeletal effects is crucial to guide clinical decisions. The randomized trial provides that rosiglitazone causes bone loss. An imbalance in fracture rates was identified in a final review of adverse event reports in ADOPT trial. That may result from the loss of bone mass due to thiazolidinedione. Animal and in vitro studies suggest that activ-tion of PPARγ promotes adipegenesis at the expense of osteoblastogenesis, and therefore inhibit bone forma-tion and induce bone loss.     

噻唑烷二酮类药物对骨骼的影响

In women,short-term clinical trials demonstrated substantial bone loss with thiazolidinedi-one. Pioglitazone and rosiglitazone are widely used to treat diabetes, and better knowledge of their skeletal effects is crucial to guide clinical decisions. The randomized trial provides that rosiglitazone causes bone loss. An imbalance in fracture rates was identified in a final review of adverse event reports in ADOPT trial. That may result from the loss of bone mass due to thiazolidinedione. Animal and in vitro studies suggest that activ-tion of PPARγ promotes adipegenesis at the expense of osteoblastogenesis, and therefore inhibit bone forma-tion and induce bone loss.     

噻唑烷二酮类药物对骨骼的影响

In women,short-term clinical trials demonstrated substantial bone loss with thiazolidinedi-one. Pioglitazone and rosiglitazone are widely used to treat diabetes, and better knowledge of their skeletal effects is crucial to guide clinical decisions. The randomized trial provides that rosiglitazone causes bone loss. An imbalance in fracture rates was identified in a final review of adverse event reports in ADOPT trial. That may result from the loss of bone mass due to thiazolidinedione. Animal and in vitro studies suggest that activ-tion of PPARγ promotes adipegenesis at the expense of osteoblastogenesis, and therefore inhibit bone forma-tion and induce bone loss.     

噻唑烷二酮类药物对骨骼的影响

In women,short-term clinical trials demonstrated substantial bone loss with thiazolidinedi-one. Pioglitazone and rosiglitazone are widely used to treat diabetes, and better knowledge of their skeletal effects is crucial to guide clinical decisions. The randomized trial provides that rosiglitazone causes bone loss. An imbalance in fracture rates was identified in a final review of adverse event reports in ADOPT trial. That may result from the loss of bone mass due to thiazolidinedione. Animal and in vitro studies suggest that activ-tion of PPARγ promotes adipegenesis at the expense of osteoblastogenesis, and therefore inhibit bone forma-tion and induce bone loss.     

噻唑烷二酮类药物对骨骼的影响

In women,short-term clinical trials demonstrated substantial bone loss with thiazolidinedi-one. Pioglitazone and rosiglitazone are widely used to treat diabetes, and better knowledge of their skeletal effects is crucial to guide clinical decisions. The randomized trial provides that rosiglitazone causes bone loss. An imbalance in fracture rates was identified in a final review of adverse event reports in ADOPT trial. That may result from the loss of bone mass due to thiazolidinedione. Animal and in vitro studies suggest that activ-tion of PPARγ promotes adipegenesis at the expense of osteoblastogenesis, and therefore inhibit bone forma-tion and induce bone loss.     

噻唑烷二酮类药物对骨骼的影响

In women,short-term clinical trials demonstrated substantial bone loss with thiazolidinedi-one. Pioglitazone and rosiglitazone are widely used to treat diabetes, and better knowledge of their skeletal effects is crucial to guide clinical decisions. The randomized trial provides that rosiglitazone causes bone loss. An imbalance in fracture rates was identified in a final review of adverse event reports in ADOPT trial. That may result from the loss of bone mass due to thiazolidinedione. Animal and in vitro studies suggest that activ-tion of PPARγ promotes adipegenesis at the expense of osteoblastogenesis, and therefore inhibit bone forma-tion and induce bone loss.     

过氧化物酶体增殖物激活受体γ与炎症性肠病

过氧化物酶体增殖物激活受体（PPAR）γ是核激素受体超家族成员，主要在脂肪组织、大肠、视网膜及部分免疫系统表达，在脂肪细胞分化、糖、脂代谢、动脉粥样硬化形成、炎性反应中发挥重要生物作用。其可能通过抑制NF-kB活化，减少促炎症细胞因子的转录及表达，从而下调过度的免疫反应，避免组织损伤。其配体主要有脂肪酸代谢产物、前列腺素、噻唑烷二酮类药物和NSAIDs等，研究报道PPARγ配体可能代表UC的新疗法。     

转移性相关基因CD44v6在结直肠癌中的表达意义

结直肠癌转移是宿主致死的主要原因之一.近年发现细胞黏附因子CD44基因表达与结直肠癌的生长、浸润、转移和预后相关.我们运用免疫组化链霉素抗生物素-过氧化酶方法(S-P法)对165例结直肠癌组织用CD44 v6单克隆抗体进行标记,探讨其与结直肠癌预后的关系.