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.     

胶囊内镜对各段小肠的诊断价值探讨

目的探讨胶囊内镜在各段小肠中的诊断价值。方法 53例受检者行严格小肠肠道清洁,采用以色列GIVEN公司的SB胶囊内镜行全小肠检查。根据小肠肠腔特点和Given定位系统,将小肠分为3段。统计各段小肠的肠道清洁度、病变检出率和评价病灶表面特征的观察效果,对影响因素进行分析。结果全部受检者完成检查。47例受检者完成全小肠观察,10例受检者共发现13处观察效果不佳,约占总受检病例数的18.9%;其中第1、第2和第3段小肠发现清洁欠清晰数分别为4、1和8,分别约占总数的31.8%、7.7%和61.5%。42例受检者发现病变,共发现病灶约75处,部分病灶表面特征观察效果欠佳。3段小肠总病灶数无明显差异,但3段小肠的非炎症病灶数的百分比分别为:16.7%、50.0%和33.3%。结论胶囊内镜检测第2段小肠有良好观察效果及病变检出率;改进检查条件有助提高胶囊内镜在第1段和第3段小肠的诊断价值。     

复方聚乙二醇电解质散在胶囊内镜检查前肠道准备的效果观察

目的:观察复方聚乙二醇电解质散对胶囊内镜检查前肠道准备的清洁效果和受检者主观感受.方法:共42例受检者,均于检查前1天20:00及检查当天5:00分别服用复方聚乙二醇电解质散,上午8:00开始检查.有便秘史者在检查前1天晚上口服果导片4片.根据清洁效果及受检者的主观感受进行综合分析.结果:全部受检者完成检查,认为能接受和无明显感觉者约占92.9%;回肠中段开始出现较多气泡或/和胆汁者39例.结论:综合清洁效果和受检者的主观感受,认为分两次口服复方聚乙二醇电解质散是比较理想的胶囊内镜检查前的肠道准备方法.     

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.     

新霉素联合双歧三联活菌片治疗肠易激综合征合并小肠细菌过度生长的疗效分析

目的探讨新霉素联合双歧三联活菌片治疗肠易激综合征合并小肠细菌过度生长的临床疗效。方法将IBS患者64例随机分为治疗组与对照组,各32例。对照组给予双歧三联活菌片口服;治疗组先给予新霉素治疗的基础上,再给予双歧三联活菌片治疗,疗程均为4周。治疗结束后,观察两组的临床疗效,并作分析。结果治疗组总有效率为84.4%高于对照组的59.4%,差异有统计学意义(P<0.05);两组均无明显药物不良反应出现。结论新霉素和双歧三联活菌片用于改善IBS的临床症状效果显著,值得临床推广应用。     

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.     

67例溃疡性结肠炎患者的随访分析

炎症性肠病(IBD)是一类病因不明的肠道非特异性炎症,包括克罗恩病(CD)和溃疡性结肠炎(UC).近20余年来IBD在中国有明显增多趋势[1-4].IBD的诊断较为困难,治疗上仍无统一模式而需个体化治疗,目前尚无可治愈的方法和药物.IBD内镜表现及预后转归的个体差别较大,影响IBD预后的因素临床报道也不一致[5,6].此研究对本院近8年确诊的67例UC患者的临床及内镜资料进行分析总结,并电话和(或)门诊随访治疗过程和预后情况,以期发现对UC治疗和预后有价值的线索.     

核因子-κBp65反义寡核苷酸对肝纤维化作用的实验研究

目的 探讨核因子(NF)-κBp65反义寡核苷酸(ASODN)对肝星状细胞(HSC)NF-κB活性和白细胞介素(IL)-6表达的影响.方法 分离培养大鼠HSC,用锥虫蓝染色法和电泳迁移位移试验(EMSA)分别检测NF-κBp65 ASODN对HSC毒性和NF-leB活性的影响,RT-PCR法和ELISA法分别检测对IL-6 mRNA和蛋白表达的影响.结果 ASODN在0.001～1.0μmol/L浓度时,对体外培养的HSC无明显毒性.HSC经肿瘤坏死因子(TNF)-α刺激后,NF-κB活性增强,在0.001～1.0μmol/L的ASODN作用后,NF-κB活性明显减弱.且呈剂量依赖性.同时转染ASODN(0.001～1.0μmol/L)后,TNF-α诱导HSC的IL-6 mRNA及蛋白表达明显降低,亦呈剂量依赖性.结论 ASODN能特异性降低NF-κB活性,同时减少HSC的IL-6表达,为其治疗肝纤维化提供了理论基础.     

核因子-κ B p65反义寡核苷酸对大鼠肝星状细胞转化生长因子β1及细胞间黏附分子1表达的影响

目的 探讨核因子-κB p65反义寡核苷酸(NF-κB 065 ASODN)对大鼠肝星状细胞HSC炎症因子转化生长因子β 1(TGF β 1)及细胞间黏附分子1(ICAM-1)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;人工合成NF-κB p65 ASODN并行全程硫代磷酸化修饰;观察脂质体介导的不同浓度的NF-κB p65 ASODN(0.001、0.010、0.100、1.000μmol/L)对肿瘤坏死因子(TNF)α刺激HSC产生TGF β1及ICAM-1 mRNA和蛋白质表达的影响,蛋白凝胶电脉迁移率变动分析法检测NF-κB p65 ASODN对TNF α刺激HSCNF-κB的活性影响.结果 TNF α刺激HSC后,NF-κB活性和TGF β1、ICAM-1的表达明显增强;应用NF-κB p65 ASODN(0.001～1.000 μmol/L)作用后,NF-κB活性明显减弱,且呈剂量依赖性,灰度值分别为16 070±223,15 715±199,14 999±224,14 447±228,各组比较,P值均<0.05.同时TGF β1、ICAM-1的mRNA及蛋白质表达明显减少,亦呈剂量依赖性,P值均<0.05.结论 NF-κB p65 ASODN可特异性降低HSC的NF-κB的活性,明显抑制TGF β1、ICAM-1的表达,为NF-κB p65 ASODN治疗肝纤维化提供了理论依据.