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1.
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. 相似文献
2.
叶石才 《心电图杂志(电子版)》2020,(2):141-142
目的探讨胃间质瘤患者实施内镜下粘膜剥离术治疗的临床疗效和安全性。方法将本院肿瘤科200例胃间质瘤患者(2017年1月-2018年6月间)纳入研究,对患者均实施内镜下粘膜剥离术治疗,分析患者手术及术后恢复指标、并发症、手术效果及预后状况。结果患者平均手术时间为(91.2±12.2)min,平均手术出血量(22.6±6.3)mL。术中穿孔率为10.0%,术中实施电凝、金属夹夹闭处理,术后效果良好。术中均未出现中转外科手术状况,手术均成功。平均术后肛门排气时间为(12.3±1.6)h;平均术后排便时间为(3.1±0.4)d;平均术后住院时间为(8.9±1.2)d。术后未出现严重并发症,仅出现1例发热患者,术后并发症总发生率为3.3%。术后肿瘤病灶残留率为0.0%,术后1年疾病复发为0.0%。结论胃间质瘤患者实施内镜下粘膜剥离术治疗效果良好,可有效切除病灶,操作较为简单,创伤较小,术后恢复较快,且复发率低,安全性高。 相似文献
3.
目的 探讨蚂蚁制剂阴阳平衡散灌肠治疗UC的作用机制.方法 溃疡性结肠炎患者82例,其中阴阳平衡散灌肠组(A组)40例和柳氮磺氨吡啶(SASP)栓剂塞肛治疗组(B组)42例,健康对照组35例,用流式细胞仪检测各组外周血及肠黏膜组织中CD+4 CD+25 Tregs细胞的变化.结果 治疗前UC患者外周血及肠黏膜组织中的CD+4 CD+25 Tregs细胞数量均显著低于健康对照组(P<0.01),而经SASP和阴阳平衡散灌肠治疗后该细胞亚群明显高于治疗前及对照组(P<0.01或P<0.05).结论 CD+4、CD+25 Tregs细胞亚群在UC的发病及病情转归中可能具有重要免疫调节作用,阴阳平衡散通过调节Tregs细胞的数量对UC发挥治疗作用. 相似文献
4.
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. 相似文献
6.
目的:探讨湿热对溃疡性结肠炎(UC)大鼠模型的影响。方法:采用内因(高脂高糖饮食)和外因(高湿高温气候)因素刺激,再辅以DNCB/乙酸灌肠建立湿热UC大鼠模型,探讨湿热对UC大鼠证候学、病理学及免疫学指标的变化。结果:湿热UC比单纯UC更早出现与大肠湿热UC患者相似的临床症状,DAI、病理学评分均升高;湿热UC血清SOD、MPO、MIF和组织TXB_2水平明显高于单纯UC(P0.05);湿热UC血清和组织MPO、P选择素、组织MIF、TXB_2与单纯UC表达水平一致,均比正常组升高。结论:血清SOD、MPO、MIF和组织TXB_2水平可作为判断湿热病因所致UC的免疫标识物;湿热能促进UC的发生和进一步加重炎症程度,是UC的主要病因。 相似文献
7.
病原生物学教学中多种教学法的综合应用,不仅可以激发医学生的学习兴趣,还可以培养医学生自主思考的创新能力。本文在分析近年来病原生物学教学改革内容及改革方向的基础上,提出了具体教学改革方法,包括搭建多媒体在线教学平台,开展线上线下混合教学法、基于“雨课堂”的案例教学法,在病原生物学实验教学课程中,引入临床相关性教学法、应用虚拟仿真及3D打印技术,实行病原生物学实验教学法等。通过多种教学法的综合应用,达到提高教学实践水平、提升学生专业能力的目的。 相似文献
8.
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. 相似文献
9.
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. 相似文献
10.
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. 相似文献