IGFBP-rP1对肝星状细胞活化及核因子-KB活性的影响

目的:明确胰岛素样生长因子结合蛋白相关蛋白1(IGFBP-rP1)是否具有活化肝星状细胞(HSC)、增加细胞外基质(ECM)合成的作用;并探讨可能的信号转导途径.方法:大鼠肝星状细胞株(HSC-T6)体外培养,分别设立空白对照组(加入等量PBS)和不同浓度的IGFBP-rPl处理组,干预因素处理24 h后收集细胞爬片或制备单细胞悬液,采用免疫细胞化学染色观察HSC-T6中Ot-平滑肌肌动蛋白(、I型胶原(colla-gen I)、纤维连接蛋白(FN)的表达变化;流式细胞仪检测HSC-T6中核因子-KB v65(NF-KB p65)的DNA结合活性.结果:免疫细胞化学染色结果发现,IGFBP-rPl各处理组、collagen I、FN的表达均较空白对照组显著增强,且在一定范围内呈剂量依赖关系;流式细胞仪检测结果显示,IGFBP-rPl各处理组NF-KB p65阳性细胞百分数均较空白对照组明显增高.结论:IGFBP-rPl可以激活HSC,且在一定剂量范围内随着IGFBP-rPl剂量的增加HSC活化的程度逐渐增强;IGFBP-rPl可使ECM的重要组成成分collagen l和FN的合成增加;IGFBP-rPl可增强HSC中NF-KB p65的DNA结合活性.     

核因子κB p65反义寡核苷酸对大鼠肝星状细胞增殖和I型胶原表达的影响

目的 探讨核因子κB(NF-κB)p65反义寡核苷酸(ASOND)对大鼠肝星状细胞(HSC)增殖和I型胶原表达的影响.方法 Ⅳ型胶原酶消化密度梯度离心法分离培养大鼠HSC;脂质体介导的不同浓度的NF-κB p65 ASOND(0.001、0.01、0.1和1μmol/L)进入HSC;台盼蓝染色排斥法检测NF-κBp65 ASOND对HSC的毒性实验并检测各组乳酸脱氢酶(LDH)活性;MTT法测定NF-κB p65 ASOND对1mg/LTNF-α刺激后HSC增殖影响;RT-PCR法和ELISA法检测不同浓度NF-κB p65 ASOND对1mg/LTNF-α刺激后HSC I型胶原表达的影响.结果 转染NF-κB p65 ASODN后,HSC细胞NF-κB蛋白的表达下降,不同浓度(0.001、0.01、0.1和1 μmol/L)的NF-κB p65 ASOND对于体外培养HSC的存活率和LDH无明显影响(P>0.05),0.01～μmol/L的NF-κB p65 ASOND抑制HSC的增殖,lmg/L TNF-α刺激HSC的I型胶原蛋白和mRNA的表达,且随浓度的增加作用增强(P<0.05).结论 NF-κB p65 ASOND可通过抑制NF-κB活性减少HSC活化增殖及Ⅰ型胶原生成,从而减少细胞外基质的产生.     

Effect of nuclear factor-κB p65 ASOND on I typ collagen expression and rat hepatic stellate cells proliferation

Objective Sstudy effect of nuclear factor-κB ASOND on I type collagen expression and rat hepatic stellate cells(HSC)proliferation.Methods Rat HSCs were separated by affusing and digestingof Ⅳ type collagenenzyme and density acentric method.Lipid-mediated NF-κB p65 ASOND(0.001,0.01,0.1,1μmol/L)Was transferred into rat HSCs.Toxicity of HSCs caused by NF-κB p65 ASOND and activity of LDH were determined by trypan blue staining.Proliferation affection of transferring NF-κB p65 ASOND into HSCs was determined by MTT.In different concentration NF-κB p65 ASOND.expression of Ⅰ type collagen stimulated by 1mg/L TNF-αwas determined by RT-PCR and ELISA.Results After transfection of NF-κB p65 ASODN,expression of NF-κB protein in HSCs was decreasing.Toxicity experiment indicated that NF-κB p65 ASOND of different concentration(0.001,0.01,0.1 and 1.0 μmol/L)had no effect on HSCs livability and LDH activity(P<0.05).Four different concentration NF-κ B p65 ASOND could restrain HSCs proliferation stimulated by 1 mg/L TNF-α.The expression of I type collagen and mRNA stimulated by 1mg/LTNF-αwas increased,and had a positive correlation with concentration(P>0.05).Conclusion NF-κB p65 ASOND may depress NF-κB activity to restrain HSCs proliferation and Ⅰ type collagen expression,and reduce extracellular matrix.     

Effect of nuclear factor-κB p65 ASOND on I typ collagen expression and rat hepatic stellate cells proliferation

Objective Sstudy effect of nuclear factor-κB ASOND on I type collagen expression and rat hepatic stellate cells(HSC)proliferation.Methods Rat HSCs were separated by affusing and digestingof Ⅳ type collagenenzyme and density acentric method.Lipid-mediated NF-κB p65 ASOND(0.001,0.01,0.1,1μmol/L)Was transferred into rat HSCs.Toxicity of HSCs caused by NF-κB p65 ASOND and activity of LDH were determined by trypan blue staining.Proliferation affection of transferring NF-κB p65 ASOND into HSCs was determined by MTT.In different concentration NF-κB p65 ASOND.expression of Ⅰ type collagen stimulated by 1mg/L TNF-αwas determined by RT-PCR and ELISA.Results After transfection of NF-κB p65 ASODN,expression of NF-κB protein in HSCs was decreasing.Toxicity experiment indicated that NF-κB p65 ASOND of different concentration(0.001,0.01,0.1 and 1.0 μmol/L)had no effect on HSCs livability and LDH activity(P<0.05).Four different concentration NF-κ B p65 ASOND could restrain HSCs proliferation stimulated by 1 mg/L TNF-α.The expression of I type collagen and mRNA stimulated by 1mg/LTNF-αwas increased,and had a positive correlation with concentration(P>0.05).Conclusion NF-κB p65 ASOND may depress NF-κB activity to restrain HSCs proliferation and Ⅰ type collagen expression,and reduce extracellular matrix.     

Effect of nuclear factor-κB p65 ASOND on I typ collagen expression and rat hepatic stellate cells proliferation

Objective Sstudy effect of nuclear factor-κB ASOND on I type collagen expression and rat hepatic stellate cells(HSC)proliferation.Methods Rat HSCs were separated by affusing and digestingof Ⅳ type collagenenzyme and density acentric method.Lipid-mediated NF-κB p65 ASOND(0.001,0.01,0.1,1μmol/L)Was transferred into rat HSCs.Toxicity of HSCs caused by NF-κB p65 ASOND and activity of LDH were determined by trypan blue staining.Proliferation affection of transferring NF-κB p65 ASOND into HSCs was determined by MTT.In different concentration NF-κB p65 ASOND.expression of Ⅰ type collagen stimulated by 1mg/L TNF-αwas determined by RT-PCR and ELISA.Results After transfection of NF-κB p65 ASODN,expression of NF-κB protein in HSCs was decreasing.Toxicity experiment indicated that NF-κB p65 ASOND of different concentration(0.001,0.01,0.1 and 1.0 μmol/L)had no effect on HSCs livability and LDH activity(P<0.05).Four different concentration NF-κ B p65 ASOND could restrain HSCs proliferation stimulated by 1 mg/L TNF-α.The expression of I type collagen and mRNA stimulated by 1mg/LTNF-αwas increased,and had a positive correlation with concentration(P>0.05).Conclusion NF-κB p65 ASOND may depress NF-κB activity to restrain HSCs proliferation and Ⅰ type collagen expression,and reduce extracellular matrix.     

Effect of nuclear factor-κB p65 ASOND on I typ collagen expression and rat hepatic stellate cells proliferation

Objective Sstudy effect of nuclear factor-κB ASOND on I type collagen expression and rat hepatic stellate cells(HSC)proliferation.Methods Rat HSCs were separated by affusing and digestingof Ⅳ type collagenenzyme and density acentric method.Lipid-mediated NF-κB p65 ASOND(0.001,0.01,0.1,1μmol/L)Was transferred into rat HSCs.Toxicity of HSCs caused by NF-κB p65 ASOND and activity of LDH were determined by trypan blue staining.Proliferation affection of transferring NF-κB p65 ASOND into HSCs was determined by MTT.In different concentration NF-κB p65 ASOND.expression of Ⅰ type collagen stimulated by 1mg/L TNF-αwas determined by RT-PCR and ELISA.Results After transfection of NF-κB p65 ASODN,expression of NF-κB protein in HSCs was decreasing.Toxicity experiment indicated that NF-κB p65 ASOND of different concentration(0.001,0.01,0.1 and 1.0 μmol/L)had no effect on HSCs livability and LDH activity(P<0.05).Four different concentration NF-κ B p65 ASOND could restrain HSCs proliferation stimulated by 1 mg/L TNF-α.The expression of I type collagen and mRNA stimulated by 1mg/LTNF-αwas increased,and had a positive correlation with concentration(P>0.05).Conclusion NF-κB p65 ASOND may depress NF-κB activity to restrain HSCs proliferation and Ⅰ type collagen expression,and reduce extracellular matrix.     

Effect of nuclear factor-κB p65 ASOND on I typ collagen expression and rat hepatic stellate cells proliferation

Objective Sstudy effect of nuclear factor-κB ASOND on I type collagen expression and rat hepatic stellate cells(HSC)proliferation.Methods Rat HSCs were separated by affusing and digestingof Ⅳ type collagenenzyme and density acentric method.Lipid-mediated NF-κB p65 ASOND(0.001,0.01,0.1,1μmol/L)Was transferred into rat HSCs.Toxicity of HSCs caused by NF-κB p65 ASOND and activity of LDH were determined by trypan blue staining.Proliferation affection of transferring NF-κB p65 ASOND into HSCs was determined by MTT.In different concentration NF-κB p65 ASOND.expression of Ⅰ type collagen stimulated by 1mg/L TNF-αwas determined by RT-PCR and ELISA.Results After transfection of NF-κB p65 ASODN,expression of NF-κB protein in HSCs was decreasing.Toxicity experiment indicated that NF-κB p65 ASOND of different concentration(0.001,0.01,0.1 and 1.0 μmol/L)had no effect on HSCs livability and LDH activity(P<0.05).Four different concentration NF-κ B p65 ASOND could restrain HSCs proliferation stimulated by 1 mg/L TNF-α.The expression of I type collagen and mRNA stimulated by 1mg/LTNF-αwas increased,and had a positive correlation with concentration(P>0.05).Conclusion NF-κB p65 ASOND may depress NF-κB activity to restrain HSCs proliferation and Ⅰ type collagen expression,and reduce extracellular matrix.     

Effect of nuclear factor-κB p65 ASOND on I typ collagen expression and rat hepatic stellate cells proliferation

Objective Sstudy effect of nuclear factor-κB ASOND on I type collagen expression and rat hepatic stellate cells(HSC)proliferation.Methods Rat HSCs were separated by affusing and digestingof Ⅳ type collagenenzyme and density acentric method.Lipid-mediated NF-κB p65 ASOND(0.001,0.01,0.1,1μmol/L)Was transferred into rat HSCs.Toxicity of HSCs caused by NF-κB p65 ASOND and activity of LDH were determined by trypan blue staining.Proliferation affection of transferring NF-κB p65 ASOND into HSCs was determined by MTT.In different concentration NF-κB p65 ASOND.expression of Ⅰ type collagen stimulated by 1mg/L TNF-αwas determined by RT-PCR and ELISA.Results After transfection of NF-κB p65 ASODN,expression of NF-κB protein in HSCs was decreasing.Toxicity experiment indicated that NF-κB p65 ASOND of different concentration(0.001,0.01,0.1 and 1.0 μmol/L)had no effect on HSCs livability and LDH activity(P<0.05).Four different concentration NF-κ B p65 ASOND could restrain HSCs proliferation stimulated by 1 mg/L TNF-α.The expression of I type collagen and mRNA stimulated by 1mg/LTNF-αwas increased,and had a positive correlation with concentration(P>0.05).Conclusion NF-κB p65 ASOND may depress NF-κB activity to restrain HSCs proliferation and Ⅰ type collagen expression,and reduce extracellular matrix.     

Effect of nuclear factor-κB p65 ASOND on I typ collagen expression and rat hepatic stellate cells proliferation

Objective Sstudy effect of nuclear factor-κB ASOND on I type collagen expression and rat hepatic stellate cells(HSC)proliferation.Methods Rat HSCs were separated by affusing and digestingof Ⅳ type collagenenzyme and density acentric method.Lipid-mediated NF-κB p65 ASOND(0.001,0.01,0.1,1μmol/L)Was transferred into rat HSCs.Toxicity of HSCs caused by NF-κB p65 ASOND and activity of LDH were determined by trypan blue staining.Proliferation affection of transferring NF-κB p65 ASOND into HSCs was determined by MTT.In different concentration NF-κB p65 ASOND.expression of Ⅰ type collagen stimulated by 1mg/L TNF-αwas determined by RT-PCR and ELISA.Results After transfection of NF-κB p65 ASODN,expression of NF-κB protein in HSCs was decreasing.Toxicity experiment indicated that NF-κB p65 ASOND of different concentration(0.001,0.01,0.1 and 1.0 μmol/L)had no effect on HSCs livability and LDH activity(P<0.05).Four different concentration NF-κ B p65 ASOND could restrain HSCs proliferation stimulated by 1 mg/L TNF-α.The expression of I type collagen and mRNA stimulated by 1mg/LTNF-αwas increased,and had a positive correlation with concentration(P>0.05).Conclusion NF-κB p65 ASOND may depress NF-κB activity to restrain HSCs proliferation and Ⅰ type collagen expression,and reduce extracellular matrix.     

Effect of nuclear factor-κB p65 ASOND on I typ collagen expression and rat hepatic stellate cells proliferation

Objective Sstudy effect of nuclear factor-κB ASOND on I type collagen expression and rat hepatic stellate cells(HSC)proliferation.Methods Rat HSCs were separated by affusing and digestingof Ⅳ type collagenenzyme and density acentric method.Lipid-mediated NF-κB p65 ASOND(0.001,0.01,0.1,1μmol/L)Was transferred into rat HSCs.Toxicity of HSCs caused by NF-κB p65 ASOND and activity of LDH were determined by trypan blue staining.Proliferation affection of transferring NF-κB p65 ASOND into HSCs was determined by MTT.In different concentration NF-κB p65 ASOND.expression of Ⅰ type collagen stimulated by 1mg/L TNF-αwas determined by RT-PCR and ELISA.Results After transfection of NF-κB p65 ASODN,expression of NF-κB protein in HSCs was decreasing.Toxicity experiment indicated that NF-κB p65 ASOND of different concentration(0.001,0.01,0.1 and 1.0 μmol/L)had no effect on HSCs livability and LDH activity(P<0.05).Four different concentration NF-κ B p65 ASOND could restrain HSCs proliferation stimulated by 1 mg/L TNF-α.The expression of I type collagen and mRNA stimulated by 1mg/LTNF-αwas increased,and had a positive correlation with concentration(P>0.05).Conclusion NF-κB p65 ASOND may depress NF-κB activity to restrain HSCs proliferation and Ⅰ type collagen expression,and reduce extracellular matrix.     

Effect of nuclear factor-κB p65 ASOND on I typ collagen expression and rat hepatic stellate cells proliferation

Objective Sstudy effect of nuclear factor-κB ASOND on I type collagen expression and rat hepatic stellate cells(HSC)proliferation.Methods Rat HSCs were separated by affusing and digestingof Ⅳ type collagenenzyme and density acentric method.Lipid-mediated NF-κB p65 ASOND(0.001,0.01,0.1,1μmol/L)Was transferred into rat HSCs.Toxicity of HSCs caused by NF-κB p65 ASOND and activity of LDH were determined by trypan blue staining.Proliferation affection of transferring NF-κB p65 ASOND into HSCs was determined by MTT.In different concentration NF-κB p65 ASOND.expression of Ⅰ type collagen stimulated by 1mg/L TNF-αwas determined by RT-PCR and ELISA.Results After transfection of NF-κB p65 ASODN,expression of NF-κB protein in HSCs was decreasing.Toxicity experiment indicated that NF-κB p65 ASOND of different concentration(0.001,0.01,0.1 and 1.0 μmol/L)had no effect on HSCs livability and LDH activity(P<0.05).Four different concentration NF-κ B p65 ASOND could restrain HSCs proliferation stimulated by 1 mg/L TNF-α.The expression of I type collagen and mRNA stimulated by 1mg/LTNF-αwas increased,and had a positive correlation with concentration(P>0.05).Conclusion NF-κB p65 ASOND may depress NF-κB activity to restrain HSCs proliferation and Ⅰ type collagen expression,and reduce extracellular matrix.     

TNF-α活化人瘢痕疙瘩成纤维细胞NF-κB的实验研究

目的：观察肿瘤坏死因子－α（TNF-α）对瘢痕疙瘩成纤维细胞（KFB）以及正常皮肤成纤维细胞（NSF）核因子-kappa B（NF-κB）的影响，以探讨瘢痕疙瘩的发生机制。 方法:原代培养成纤维细胞；免疫荧光技术观察NF-κB p65和IκB-α在静息状态和TNF-α刺激后的成纤维细胞中分布；应用TransAMTM NF-κB p65 kit试剂盒检测NF-κB p65 DNA结合活性；应用Western blotting检测IκB-α蛋白水平。 结果: TNF-α刺激后，NF-κB p65从细胞浆转移至细胞核；NF-κB p65 DNA结合活性水平在刺激后1 h达到高峰，4 h接近正常；细胞浆IκB-α蛋白水平在刺激后15 min降至最低值，4 h基本接近正常；KFB较NSF对TNF-α的刺激更为敏感。结论: KFB较NSF对TNF-α活化 NF-κB更为敏感, 可能是瘢痕疙瘩形成的潜在发病机制。     

二甲双胍对兔动脉粥样硬化NF-κB表达及血清高敏C反应蛋白水平的影响

目的： 研究二甲双胍对动脉粥样硬化家兔主动脉血管壁中NF-κB、IκBα表达和血清中高敏C反应蛋白（hs－CRP）浓度的影响，探讨其可能的抗动脉粥样硬化机制。方法:24只新西兰大耳白兔随机分为3组：空白对照组（control组）、粥样硬化组（AS组）和二甲双胍治疗组（Met组）。采用免疫内皮损伤加高胆固醇饮食的方法复制家免动脉粥样硬化模型并经升主动脉高频超声证实，然后Met组给予二甲双胍150 mg·kg-1·d-1喂养8周,至第16周实验结束时抽血检测血脂、血清高敏C反应蛋白（hs-CRP）,分别采用免疫组织化学和Western blotting方法检测家兔主动脉中NF-κB p65亚基及其抑制蛋白IκBα的表达。 结果:与control组相比，AS组血清〖JP2〗hs-CRP显著增高（1.27±0.43 vs 3.96±0.63,P<0.01），主动脉血管壁中胞核NF-κB p65亚基表达增强（P<0.01）、〖JP〗胞浆IκBα表达明显减弱（P<0.01）；与AS组比较，Met组血清hs-CRP明显降低（2.79±0.40 vs 3.96±0.63,P<0.05），胞核NF-κB p65亚基表达减弱（P<0.05）、胞浆IκBα表达增强（P<0.05）。结论：二甲双胍能够抑制动脉粥样硬化家兔血管壁中IκB的降解和NF-κB的活化，并降低血清中hs-CRP，提示二甲双胍具有抗炎症作用，可能是其抗动脉粥样硬化的机制之一。     

CD154(CD40L)诱导人Ramos B淋巴细胞株中转录因子NF-κB活化研究

目的 对CD40配体CD154(CD40L)在人B淋巴细胞中刺激转录因子NF-κB活化进行研究。方法应用重组CD154刺激EBV／LMP1阴性人Ramos B细胞，观察对NF-κB luciferase(萤光素酶)活化的作用，判断CD154刺激对NF-κB抑制蛋白IκB-α、-β及-ε磷酸化和降解的影响，并对CD154刺激诱导进入细胞核NF-κB亚单位进行分析。结果 CD154刺激：(1)导致NF-κB lucfferase活性升高，且与CD154剂量正相关；(2)引起细胞内IκB-α、-β及-ε蛋白总量减少，IκB-α、-β及-ε阳性细胞也明显减少；(3)主要诱导p50、p65及c-Rel亚单位从细胞浆进入细胞核；(4)诱导p65磷酸化。结论 在人Ramos B细胞中，CD154通过诱导IκB-α、-β及-ε降解释放p50、p65及c-Rel进入细胞核及p65磷酸化激活NF-κB。     

大鼠血管新生内膜形成过程中NF-κB的活化和ICAM-1及COX-2表达的变化

目的：探讨大鼠血管内膜增生过程中NF-κB活化与内膜炎性增生的相互关系。方法:Western blotting分析血管壁中NF-κB p65、IκBα及其下游炎性基因ICAM-1和COX-2的表达；用免疫沉淀分析检测NF-κB p65的苏氨酸磷酸化。结果:内皮剥脱后，血管总蛋白与核蛋白中p65的含量于术后7 d达峰值；术后21 d下降但仍高于0、1 d组；但胞浆p65含量无明显变化。p65苏氨酸磷酸化水平与NF-κB核转位成负相关关系。IκBα于术后1 d表现出一过性降低，术后14 d开始回升，21 d接近正常组水平；与此相反，ICAM-1和COX-2的表达于内皮剥脱后升高，至14 d时达峰值，21 d时表达量下降但仍高于正常组。结论:血管内皮剥脱诱导的内膜增生过程中伴有持续的NF-κB p65活化和炎性因子的表达。     

五味子多糖对TGF-β1诱导的人肾小球系膜细胞炎症因子和细胞外基质FN和COLⅠ表达的影响

目的：探讨五味子多糖（SCP）对TGF-β1诱导的人肾小球系膜细胞炎症因子和细胞基质（ECM）表达的影响。方法：体外培养人肾小球系膜细胞，采用4 ng/ml TGF-β1诱导人肾小球系膜细胞构建系膜增生性肾炎细胞模型，分为正常对照（Con）组、模型（TGF-β1）组、SCP低、中、高浓度（SCP-L、SCP-M、SCP-H）组，MTT检测细胞增殖活性，ELISA检测炎症细胞因子IL-6、IL-1β、TNF-α和单核细胞趋化蛋白1(MCP-1)含量，qRT-PCR和Western blot分析纤连蛋白（FN）和Ⅰ型胶原蛋白（COLⅠ）表达，Western blot评估TLR4/NF-κB信号传导途径关键蛋白表达。结果：与Con组相比，TGF-β1组细胞增殖活性明显升高，IL-6、IL-1β、TNF-α和MCP-1含量明显升高，FN、COLⅠ、Toll样受体4(TLR4)、髓样分化因子（MyD88）和磷酸化核因子-κB p65(p-NF-κB p65)表达明显上调（P<0.05）；与TGF-β1组相比，不同浓度SCP干预均能够抑制细胞增殖活性，降低IL-6、IL-1β、TNF-α和M...     

大黄素通过抑制NF-κB信号通路改善骨关节炎的软骨降解分析

目的：探讨大黄素在改善骨关节炎软骨降解中的作用及机制。方法：大黄素（20μmol/L）预处理SD大鼠软骨细胞2 h,IL-1β(10 ng/ml)孵育24 h。MTT检测不同处理组细胞活力,RT-PCR和Western blot分析aggrecan、collagenⅡ、MMP-13、ADAMTS-4、NF-κB p65、IKK-β、IκB-α表达。结果：与IL-1β组相比,IL-1β+大黄素组大鼠软骨细胞aggrecan和COL2A1 mRNA水平显著升高（P<0.05）,MMP-13、ADAMTS-4、NF-κB p65和IKK-β mRNA水平显著降低（P<0.05）,而IκB-α mRNA水平显著升高（P<0.05）。结论：大黄素通过抑制NF-κB途径抑制MMP和ADAMTS表达,从而发挥软骨保护作用。     

沙立度胺对大鼠肝纤维化核因子-κB和肿瘤坏死因子-α表达的影响

目的： 观察沙立度胺抗大鼠肝纤维化的疗效和对NF-κB和TNF-α表达的影响。方法： 四氯化碳腹腔注射诱导大鼠肝纤维化模型，治疗组于造模同时用沙立度胺10 mg·kg^-1·d^-1和100 mg·kg^-1·d^-1灌胃8周。观察肝组织病理学改变，检测肝功能、血清肝纤维化指标及肝组织羟脯氨酸含量，免疫组化检测NF-κB p65、α-SMA 在肝内的表达和分布，Western blotting检测肝组织NF-κB p65、IκBα、TNF-α蛋白的表达，RT-PCR检测肝组织TNF-α mRNA表达。结果： 高剂量沙立度胺治疗组肝脏炎症及纤维化程度低于模型组；其ALT、AST水平,HA、LN及羟脯氨酸含量，肝组织细胞核NF-κB p65和肝组织α-SMA蛋白表达，以及肝组织TNF-α mRNA和蛋白表达均低于模型组(P<0.01）；而PA水平和细胞质中IκBα蛋白表达高于模型组(P<0.01)。结论： 沙立度胺可有效地抑制实验性大鼠肝纤维化的发展，通过抑制IκB解离和降解从而减弱NF-κB通路对TNF-α表达的诱导可能是它发挥疗效的机制之一。     

LPS致大鼠肺泡巨噬细胞NF-κB促进TNF-α分泌

目的: 观察脂多糖（LPS）致大鼠肺泡巨噬细胞（AMs）中核因子NF-κB活性及其调控肿瘤坏死因子-α（TNF-α）分泌的作用。 方法: LPS作用大鼠AMs后，用电泳迁移率改变分析法（EMSA）测NF-κB活性；用特异的反义寡核苷酸阻断NF-κB亚基（p65）后，Western blotting检测p65表达变化；ELISA法检测细胞上清中TNF-α的含量。 结果: 于LPS作用AMs后4 h，NF-κB活性达到峰值，24 h仍维持在高水平；作用后4 h上清中TNF-α的含量达到峰值。反义寡核苷酸阻断NF-κB亚基（p65）表达后，LPS致AMs上清中TNF-α的含量显著低于未阻断组（P<0.01）。结论: LPS致大鼠AMs中NF-κB正向调控TNF-α分泌。     

NBD多肽预处理对局灶脑缺血再灌注大鼠脑内核因子-κB核转位活化的影响

目的探讨NBD多肽预处理对局灶脑缺血再灌注大鼠大脑缺血皮质细胞内核因子-κB活化的影响。方法将SD健康雄性大鼠（280～300g）共36只随机分为假手术组（n=6）、模型组（n=15）、药物组（n=15）。缺血模型制备前2h经右侧侧脑室注射NBD多肽25μl进行预处理。运用改良线栓法制备右侧大脑中动脉闭塞再灌注大鼠模型。运用免疫组化检测再灌注后72hNF-κBp65在胞浆／胞核的蛋白表达变化;运用免疫荧光定位及Western印迹（半定量）检测NF-κB p65及IκBα的蛋白表达情况。结果免疫组化结果显示与假手术组比较,再灌注72h模型组胞浆／胞核内NF-κB p65大量表达（P〈0．05）;NBD多肽预处理后NF-κB p65主要在胞浆表达,胞核内表达明显减少（P〈0．05）;免疫荧光双标定位及Western印迹半定量检测显示模型组胞浆／胞核内NF-κB p65蛋白均大量表达（P〈0．05）,IκBα蛋白呈现低表达（P〈0．05）;NBD多肽预处理后胞核内NF-κB p65蛋白表达明显减少,主要以胞浆表达为主（P〈0．05）,IκBα胞浆／胞核内表达显著增加（P〈0．05）。结论局灶脑缺血再灌注72hNF-κB p65蛋白胞核表达明显增加．NF-κB核转位／活化过程被激活：NBD多肽预处理后通过增加胞核／胞浆内IκBα表达有效阻止NF-κB的核转位／活化过程,从而有效地减轻再灌注后72h局灶脑缺血再灌注对脑组织的损害。