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c-erbB2、nm23-H1在妊娠滋养细胞疾病中的表达及其临床意义

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实用妇产科杂志 2003年第4期19卷 216-218页

作者：王玉霞孙永玉徐州医学院附属医院江苏徐州221002 华中科技大学同济医学院附属协和医院湖北武汉430022

目的 :探讨癌基因c erbB2和抑癌基因nm2 3 H1在妊娠滋养细胞肿瘤的临床分期及临床主要预后因素不同的情况下表达的差异 ,以期达到对妊娠滋养细胞疾病转归的预测。方法 :采用针对两种基因表达产物的单克隆抗体进行SABC免疫组织化学染色 ... 详细信息

目的 :探讨癌基因c erbB2和抑癌基因nm2 3 H1在妊娠滋养细胞肿瘤的临床分期及临床主要预后因素不同的情况下表达的差异 ,以期达到对妊娠滋养细胞疾病转归的预测。方法 :采用针对两种基因表达产物的单克隆抗体进行SABC免疫组织化学染色 ,回顾性检测分析 30例不同妊娠期正常胎盘、2 1例葡萄胎、2 1例侵蚀性葡萄胎及 2 0例绒癌中两种基因产物的表达情况。结果 :c erbB2基因在侵蚀性葡萄胎和绒癌中的表达明显高于葡萄胎及妊娠中晚期正常胎盘 ,而nm2 3 H1的表达明显低于葡萄胎及妊娠中晚期正常胎盘 (P 2基因在临床Ⅲ、Ⅳ期患者中的表达高于Ⅰ、Ⅱ期患者 ,但差异无统计学意义 ;nm2 3 H1基因产物的高表达与WHO预后评分系统的好的预后因素相一致。结论 :c erbB2的高表达及nm2 3 H1的低表达与葡萄胎恶变紧密相关 ,对于妊娠滋养细胞肿瘤的早期诊断、早期治疗及预后评估具有重要的临床意义。

关键词：妊娠滋养细胞肿瘤 c-erbB2基因 nm23-H1基因免疫组织化学预后

慢性粒细胞白血病急变与bcr/abl,p53,p16基因相关性研究

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武汉大学学报：自然科学版 2001年第2期47卷 213-216页

作者：李慧玉邹国林邹平武汉大学生命科学学院湖北武汉430072 华中科技大学同济医学院协和医院湖北武汉430022

应用 RT- PCR、PCR- SSCP方法对 33例慢性粒细胞白血病 (Chronic myeloid leukem ia,CML)进行了bcr/ abl,p5 3,p16基因检测 .发现 33例 CML 中 32例 bcr/ abl基因阳性 (97.0 % ) ,2 2例慢性期无 p5 3基因突变 ,而11例急变组中一例外显... 详细信息

应用 RT- PCR、PCR- SSCP方法对 33例慢性粒细胞白血病 (Chronic myeloid leukem ia,CML)进行了bcr/ abl,p5 3,p16基因检测 .发现 33例 CML 中 32例 bcr/ abl基因阳性 (97.0 % ) ,2 2例慢性期无 p5 3基因突变 ,而11例急变组中一例外显子 5和一例外显子 7发生 p5 3基因突变 ,且均发生于急粒变组 ,2例出现 p16基因纯合缺失 ,且均发生在急淋变组 ,33例 CML 均未见 p16基因突变 .结果提示 :bcr/ abl基因与 CML 发生有关 ,而 p5 3基因突变可能与 CML 急粒变有关 ,p16纯合缺失可能与 CML

关键词： bcr/alb基因 p53基因 p16基因慢性粒细胞白血病急变基因突变基因纯言缺失

左旋咪唑诱导实验性变态反应性脑脊髓炎大鼠脊髓内单个核细胞上CD4，CD28和CD152表达的实验研究

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时珍国医国药 2008年第6期19卷 F0003-F0004页

作者：李侃李彬何家富龚权张燕翔张道明郑晓娟丁建中长江大学医学院湖北荆州434000 华中科技大学同济医学院附属协和医院湖北武汉430022 华中科技大学同济医学院附属襄樊医院湖北襄樊441021

目的观察左旋咪唑(LMS)对实验性变态反应性脑脊髓炎(EAE)大鼠脊髓内单个核细胞上CD4,CD28和CD152表达的影响,并探讨LMS诱发炎性脱髓鞘白质脑病发病机制。方法采用流式细胞术检测EAE大鼠脊髓单个核细胞上CD4,CD28和CD152的表达水平。结果... 详细信息

目的观察左旋咪唑(LMS)对实验性变态反应性脑脊髓炎(EAE)大鼠脊髓内单个核细胞上CD4,CD28和CD152表达的影响,并探讨LMS诱发炎性脱髓鞘白质脑病发病机制。方法采用流式细胞术检测EAE大鼠脊髓单个核细胞上CD4,CD28和CD152的表达水平。结果LMS同时给药组和预处理的EAE组大鼠脊髓内单个核细胞上CD4和CD28的表达水平,均明显高于非LMS处理的EAE模型组。结论LMS能促进EAE大鼠脊髓内单个核细胞上CD4和CD28的表达,提示LMS上调CD4和CD28的表达与可能LMS诱发的炎性脱髓鞘白质脑病有关。

关键词：左旋咪唑实验变态反应性脑脊髓炎

NMDA and AMPA receptors mediate intracellular calcium increase in rat cortical astrocytes

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Acta Pharmacologica Sinica 2004年第6期25卷 12-18页

作者： Bo HU, Sheng-gang SUN2, E-tang TONGNeurology Department, union hospital, tongji college, huazhong university of science and technology, wuhan 430022, china Neurology Department Union Hospital Tongji College Huazhong University of Science and Technology Wuhan 430022

AIM: To study the effect of glutamate on the intracellular calcium signal of pure cultured rat astrocytes and the roleof N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) re-ceptors in the procedure. METHODS: The fluorescence of calcium was measured by Fura-2/AM (F345/F380).RESULTS: L-Glutamate induced [Ca2+]i increase in most of the cells in concentration- and time-dependent *** 50 mmol/L induced the fluorescence increase by almost three to four times, while the effect of AMPA 50mmol/L was just half of that of D-(-)-2-amino-5-phosphonopentanoic acid (D-AP-5; a selective antagonist of theNMDA receptor). 6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX, a selective antagonist of the AMPA receptor)abolished the effects of NMDA and AMPA, respectively. D-AP-5 and CNQX simultaneously or respectively attenu-ated the effect of L-glutamate at different degrees, but could not abolish it entirely. CONCLUSION: Glutamatemodulated intracellular Ca2+ of pure cultured rat astrocytes through different pathways. The activation of NMDAand AMPA receptors took part in the complex mechanisms.

关键词： glutamate astrocytes NMDA receptors AMPA receptors calcium

Expression and signifi cance of TLR4 and HIF-1α in pancreatic ductal adenocarcinoma

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World Journal of Gastroenterology 2010年第23期16卷 2881-2888页

作者： Jian-Jun Zhang,He-Shui Wu,Lin Wang,Yuan Tian,Jing-Hui Zhang,Hai-Long Wu Department of Pancreatic Surgery,union hospital,tongji medical college,huazhong university of science and technology,wuhan 430022,Hubei Province,china Department of Pediatrics,union hospital,tongji medical college,huazhong university of science and technology,wuhan 430022,Hubei Province,china Laboratory of General Surgery,union hospital,tongji medical college,huazhong university of science and technology,wuhan 430022,Hubei Province,china Department of Pancreatic Surgery Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan 430022 Hubei Province China.

AIM:To investigate the expression of toll-like receptor(TLR) 4,nuclear factor-κB(NF-κB) p65 and hypoxiainducible transcription factor 1α(HIF-1α) in pancreatic ductal adenocarcinoma and their clinical ***:The mRNA of TLR4 and HIF-1α were investigated by real-time polymerase chain reaction in 30 cases of pancreatic ductal adenocarcinoma and its adjacent tissues,and expression of TLR4,NF-κB p65 and HIF-1α protein were detected by immunohistochemistry in 65 cases of pancreatic ductal adenocarcinoma tissues and 38 cases of corresponding adjacent *** relationship between TLR4 or HIF-1α and pathologic features,as well as the association between TLR4 and HIF-1α,were also ***-Meier method was used to assess the impact of expression of TLR4 and HIF-1α on survival of patients with pancreatic ***:The relative quantif ication of TLR4 and HIF-1α mRNA in tumor tissues was 0.81±0.10 and 0.87±0.11,respectively,signif icantly higher than that in adjacent tissues(0.81±0.10 vs 0.70±0.16,P=0.002;0.87±0.11 vs 0.68±0.13,P=0.000).The protein expression of TLR4,NF-κB p65 and HIF-1α in tumor tissues was 69.20%,66.15% and 70.80%,respectively,being signif icantly higher than that in adjacent normal tissues(69.20% vs 39.50%,P=0.003;66.15% vs 31.58%,P=0.001;70.80% vs 36.80%,P=0.001).There was no signif icant correlation between TLR4 or HIF-1α expression and the age,gender,tumor location,the degree of tumor differentiation in the patients(P>0.05).However,there was signif icant correlation between the expression of TLR4 or HIF-1α and tumor size,lymph node metastasis,venous invasion and clinical staging(P<0.05).The expression of TLR4 and HIF-1α had a signif icant impact on survival of patients with pancreatic ***:TLR4,NF-κB p65 and HIF-1α are overexpressed in pancreatic adenocarcinoma,TLR4 may be partly involved in up-regulating HIF-1α,and both synergestically promote development of pancreatic adenocarcinoma.

关键词： Pancreatic ductal adenocarcinoma Toll-like receptor 4 Nuclear factor-κB p65 Hypoxia-inducible factor 1

Deguelin inhibits expression of IκBα protein in Raji and U937 cells

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Acta Pharmacologica Sinica 2006年第4期27卷 485-490页

作者： Wei-hua CHEN Yan CHEN~2 Guo-hui CUI Department of Hematology,union hospital.tongji medical college,huazhong university of science and technology,wuhan 430022,china Department of Hematology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China

Aim:To determine whether deguelin can regulate the expression of nuclear factorkappa B(NF-κB)binding protein(IκBα)in U937 human leukemia cells and Rajihuman B lymphoma ***:The localization of IκBα protein was investi-gated by using an immunofluorescence *** expression of IκBα and NF-κB/p65 proteins in Raji and U937 cells were investigated by using Western *** was detected through annexin V/PI double-labeled ***:IκBα localized in the cytoplasm in untreated and deguelin-treated *** with tumor necrosis factor α(TNF-α)or deguelin plus TNF-α for 15 min,there was a substantial reduction in the amount of IκBα *** expressionof IκBα was downregulated by deguelin in Raji and U937 *** inducedapoptosis in U937 ***:Deguelin inhibited the expression of IκBαprotein in U937 and Raji *** anti-proliferative activity of deguelin is relatedto the signal pathway of NF-κB.

关键词： deguelin IkBα nuclear factor kappa B tumor necrosis factor-α apoptosis Raji cells U937 cells

TLR4 signaling induced TLR2 expression in the process of mimic cerebral ischemia/reperfusion in vitro

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中国科学：生命科学英文版 2010年第2期53卷 223-228页

作者： SUN Peng1,ZHANG Qing2,HAN JiYuan1,TIAN Yuan3 & ZHANG JingHui3 1Department of Emergency,union hospital,tongji medical college,huazhong university of science and technology,wuhan 430022,china 2Department of Anesthesia,union hospital,tongji medical college,huazhong university of science and technology,wuhan 430022,china 3Department of General Surgery,union hospital,tongji medical college,huazhong university of science and technology,wuhan 430022,china Department of Emergency Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China Department of Anesthesia Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China Department of General Surgery Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China

Both TLR4 and TLR2 participated in the mediation of the inflammatory injury in the process of partial cerebral ischemia/***,it still remains unclear whether a crosstalk exists between TLR2 and TLR4 in ischemic cerebral *** the present study,we investigated the effect of TLR4 signaling on TLR2 expression during mimic cerebral I/R in ***-2 cells were cultured and treated with ischemia/reperfusion,then transfected with the plasmid pEGFP-H1/TLR4-siRNA,the plasmid pEGFP-H1/control sequence-siRNA and the blank plasmid,***,the expression of TLR2 and TLR4 mRNA and protein,NF-κB p65 mRNA and supernatant TNF-α level were significantly higher in ischemia/reperfusion treated cells than those lack of ischemia/reperfusion treatment,and as compared with those in ischemia/reperfusion treated cells without transfection,no significant differences about the above mentioned gene and protein expression were found in the blank plasmid tranfected cells and the plasmid pEGFP-H1/control sequence-siRNA transfected cells respectively,while the expression levels in the plasmid pEGFP-H1/TLR4-siRNA transfected cells were significantly ***,in order to determine the effects of pyrrolidinediethyldithiocarbamate (PDTC),an NF-κB inhibitor,on the TLR4-induced TLR2 expression in BV-2 cells treated with ischemia/reperfusion,it was found that TLR4 and TLR2 mRNA expressions in PDTC pretreated cells were significantly lower in comparison with normal saline pretreated cells and non-pretreated *** data suggested that TLR2 activation,signaled by TLR4 and regulated by NF-κB,might be directly involved play an important role in ischemia/reperfusion induced brain damage.

关键词： Toll-like receptor 4 Toll-like receptor 2 cerebral ischemia/reperfusion microglia

Inhibition of ethanol-induced toxicity by tanshinone ⅡA in PC12 cells

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Acta Pharmacologica Sinica 2006年第6期27卷 659-664页

作者： Xian-fang MENG~2 Xiao-jing ZOU~3 Bin PENG~2 Jing SHI~2 Xin-min GUAN~2 Chun ZHANG~(4,5)2 Department of Neurobiology,tongji medical college,huazhong university of science and technology,wuhan 430030,china 3 Department of Anesthesiology,4 Department of Nephrology,union hospital,tongji medical college,huazhong university of science and technology,wuhan 430022.china Department of Neurobiology Tongji Medical College Huazhong University of Science and Technology Wuhan China Department of Anesthesiology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China Department of Nephrology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China

Aim:To observe the effects of tanshinone IIA(Tan IIA)on the neurotoxicityinduced by ethanol in PC 12 cells and to explore its protective ***:PC 12cell survival was measured by MTT *** formation of reactive oxygenspecies(ROS)and lactate dehydrogenase(LDH)release were detected by 2′,7′-dichlorofluorescin(DCF)fluorescence and calorimetric method,*** of cell apoptosis was monitored by flow *** expression ofp53 was detected by immuno-fluorescence and flow ***:Ethanolsignificantly impaired the survival of PC12 cells as demonstrated by MTT *** also induced significant ROS formation and increased LDH ***-incubation with Tan IIA in the culture medium significantly reversed these *** caused cell apoptosis and the upregulation of p53 *** anti-apoptosis effects of Tan IIA on ethanol-induced toxicity were accompanied by thedownregulation of pro-apoptotic p53 protein ***:Tan IIAcan protect neurons from apoptosis and might serve as a potential therapeuticdrug for neurological disorders induced by ethanol.

关键词： apoptosis ethanol PC12 cells p53 tanshinone ⅡA

Deguelin regulates nuclear pore complex proteins Nup98 and Nup88 in U937 cells in vitro1

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Acta Pharmacologica Sinica 2005年第10期26卷 1265-1273页

作者： Hong-li LIU~2, Yan CHEN~(2,3), Guo-hui CUI~2, Qiu-ling WU~2, Jing HE~2, Wei-hua CHEN~2, Jian-feng ZHOU~4 ~2 Department of Hematology, union hospital, tongji medical college, huazhong university of science and technology, wuhan 430022 ~4 Department of Hematology, tongji hospital, tongji medical college, huazhong university of science and technology, wuhan 430030, china Department of Hematology Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China Department of Hematology Tongji Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan China

Aim: To investigate the anticancer effects and the molecular mechanisms of deguelin on human U937 leukemia cells, and to explore the underlying mechanism regulating nucleoporin 98 （Nup98） and nucleoporin 88 （Nup88） in vitro. Methods: The effects of deguelin on the growth of U937 cells were studied by MTT assay. The effect of deguelin on the cell cycle of U937 cells was studied by using a propidium iodide method. The localization of the nuclear pore complex proteins Nup98 and Nup88 was investigated by using immunofluorescence and immunoelectron microscopy. The expression of Nup98 and Nup88 in U937 cells was investigated by using flow cytometry and Western blot. Results: The prolif eration of U937 cells was inhibited in the deguelin-treated group, with a 24-h IC50value of 21.61 nmol/L and a 36-h IC50value of 17.07 nmol/L. U937 cells treated with deguelin had reduced percentages of cells in the G0/G1phase, whereas cells accumulated in the S and G2/M phases. Nup88 and Nup98 were found on both the nuclar and cytoplasmic sides of the U937 cells by using immunofluorescence and immunoelectron microscopy. The expression of Nup98 was upregulated and that of the Nup88 protein was downregulated in U937 cells treated with deguelin. Conclusion: Deguelin is able to inhibit the proliferation of U937 cells by regulating the cell cycle such that cells are arrested at the S and G2/M phases, so that the proportion of cells in the G0/G1phase decreases. The antitumor effects of deguelin are related to upregulating the expression of Nup98 and downregulating the expression of Nup88 protein in U937 cells.

关键词： deguelin U937 cells nucleoporin Nup98 Nup88