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腹膜透析是终末期肾病患者的主要治疗方式之一,因有能更好地保护残余肾功能等优势,具有广泛的应用前景。但长期腹膜透析容易出现多种并发症,其中腹膜透析相关性腹膜炎是最常见的并发症之一,反复发生的炎症刺激会加速腹膜纤维化的发展,最终导致超滤衰竭,腹膜透析失败。MicroRNA(miRNA)属于非编码RNA的一种,在炎症及纤维化过程中的作用备受关注,众多miRNA参与了腹膜炎症及纤维化过程。新近研究显示,腹膜透析过程中,多种miRNA的表达谱发生了改变。该文就miRNA在腹膜透析中的研究进展进行综述。 相似文献
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Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献
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Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献
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Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献
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h后p-STAT1表达明显升高,持续至24 h,与对照组相比,差异有统计学意义(P<0.01).LPS作用4、8 h时大鼠腹水中IL-6浓度显著增高,与对照组相比差异均有统计学意义(P<0.01,P<0.05),12 h后其浓度接近对照组水平.壁层腹膜石蜡切片Masson染色可见LPS作用不同时间组腹膜组织明显水肿;各组间腹水白细胞计数差异无统计学意义.结论 腹膜组织PPAR-γ、TLR4的高表达及STAT1活化共同参与了LPS诱导的大鼠腹膜透析相关性急性腹膜炎症过程. 相似文献
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目的探讨硒对肾间质纤维化大鼠肾组织结缔组织生长因子(CTGF)表达及肾小管上皮细胞表型转化的影响。方法以单侧输尿管结扎致肾间质纤维化大鼠模型。将54只SD大鼠随机分为假手术组(A组)、单侧输尿管梗阻(UUO)组(B组)、U-UO+硒组(C组),每组18只。C组给予亚硒酸钠0.2mg/(kg·d)灌胃。A、B组给予同等剂量0.9%氯化钠溶液灌胃。术后第7、14、21天各组随机处死6只大鼠,肾组织行HE、Masson染色评定肾间质纤维化程度,免疫组织化学半定量法检测CTGF和α-平滑肌肌动蛋白(α- SMA)的表达。Western印迹法检测肾组织CTGF蛋白表达。化学比色法检测肾组织氧化指标谷胱甘肽过氧化物酶(GSH- Px)、超氧化物歧化酶(SOD)、丙二醛(MDA)的表达水平。结果术后各时点C组肾间质纤维化程度较B组明显减轻(P<0.05),肾组织CTGF和α- SMA的表达强度明显低于B组(P<0.05或0.01)、GSH- Px和SOD水平明显高于B组(P<0.05),MDA含量明显低于B组(P<0.05)。B组肾组织中CTGF、a- SMA表达量之间呈正相关(P<0.05),CTGF和a- SMA表达量与肾间质纤维化病变程度呈正相关(P<0.05)。结论硒可以减轻UUO模型大鼠肾间质纤维化程度,其机制可能与硒的抗氧化作用、下调肾组织CTGF的表达、抑制肾小管上皮细胞-肌成纤维细胞转分化有关。 相似文献
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PPARγ激动剂对腹膜透析相关性急性腹膜炎大鼠PPARγ、Toll样受体4表达及STAT1信号活化的影响 总被引:10,自引:10,他引:0
目的 观察过氧化物酶体增殖物活化受体γ(PPARγ)激动剂罗格列酮和15脱氧前列腺素J2(15d-PGJ2)对脂多糖(LPS)诱导大鼠腹膜透析相关性急性腹膜炎模型腹膜组织PPARγ、Toll样受体4(TLR4)表达、STAT1活化及腹腔局部炎性反应的影响。 方法 24只雄性SD大鼠随机分成4组,每组6只。对照组:腹腔注入4.25%葡萄糖乳酸盐腹膜透析液(简称腹透液,90 ml/kg);LPS组:LPS 1 mg/kg腹腔注入4 h后,再注入腹透液;罗格列酮+ LPS组(罗格列酮组):罗格列酮20 mg8226;kg-18226;d-1灌胃预处理3 d,注入LPS及腹透液;15d-PGJ2 + LPS组(15d-PGJ2组):15d-PGJ2 0.3 mg8226;kg-18226;d-1腹腔注入预处理3 d,注入LPS及腹透液。注入腹透液4 h后处死大鼠,留取腹水、壁层及脏层腹膜组织。ELISA法检测腹水中IL-6浓度。常规行腹膜组织Masson染色和腹水白细胞计数。RT-PCR检测腹膜组织PPARγ、TLR4 mRNA的表达;Western印迹法检测腹膜组织PPARγ、TLR4、磷酸化(p)-STAT1、STAT1蛋白的表达。 结果 LPS组大鼠腹水IL-6浓度[268.53(201.87~335.19) ng/L]高于对照组[147.62(130.60~164.64) ng/L)](P < 0.01);罗格列酮组大鼠腹水IL-6浓度[110.20(77.60~142.80) ng/L]低于LPS组(P < 0.05)。与对照组比较,LPS组大鼠腹膜组织明显水肿,腹膜组织PPARγ、TLR4 mRNA及蛋白表达均显著增强(P < 0.05)。与LPS组相比,罗格列酮组大鼠腹膜组织水肿明显减轻,PPARγ、TLR4 mRNA表达显著增高(P < 0.05),但其蛋白表达显著减弱(P < 0.05)。15d-PGJ2组大鼠腹膜组织水肿明显减轻,PPARγ mRNA及其蛋白表达均显著减弱(均P < 0.05),TLR4 mRNA表达显著增强(P < 0.01),但其蛋白表达减弱(P < 0.05)。各组间腹水白细胞计数差异无统计学意义。罗格列酮、15d-PGJ2均明显上调LPS诱导的p-STAT1表达(P < 0.01)。 结论 罗格列酮和15d-PGJ2可负性调节LPS诱导的大鼠急性腹膜炎性反应,并对LPS信号通路中相关功能蛋白起一定的调控作用。 相似文献
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Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献
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Objective To investigate the effect and mechanism by which PPARγ ligand, rosiglitasone, regulates the expression of CD40 and intercellular adhesion molecule 1 (ICAM-1) in the rat peritoneal mesothelial cells (RPMCs) induced by lipopolysaccharide (LPS). Methods RPMCs were harvested from Sprague-Dawley rat peritoneal cavity and maintained under defined in vitro conditions. The cells were randomly divided into groups as follows: medium, LPS (5 mg/L), LPS (5 mg/L)+BAY11-7085(5 μmol/L, NF-κB inhibitor), rosiglitazone (10 μmol/L or 20 μmol/L, peroxisome proliferator-activated receptor γ activator), LPS (5 mg/L)+rosiglitazone (10 μmol/L)+GW9662 (3 μmol/L, peroxisome proliferator-aetivatcd receptor γ antagonist), and LPS (5 mg/L)+vehicle (DMSO 0.2 ml/L). The expressions of CD40 and ICAM-1 RNA in RPMCs were examined by RT-PCR after 3 hour treatment, and the protein expressions of CD40, ICAM-1, p-NF-κB p65 and p-IκBα were examined by Western blot or immunofluorescence after 24 hour treatment. Results Following treatment with LPS, both the expressions of CD40 and ICAM-1 protein in RPMCs were up-regulated significantly (P<0.05), and the phosphoralation of p65 was increased greatly (1.10±0.17 vs 0.55±0.06, P<0.05). BAY11-7085 (5 μmol/L) significantly decreased the protein expression of p-p65 (0.22±0.11 vs 1.10±0.17, P<0.01), CD40 (0.34±0.02 vs 0.50±0.06, P<0.05) and ICAM-1 (0.35±0.16 vs 0.74±0.03, P<0.05). Pretreated with rosiglitazone for 3 h then added with LPS for 1 h, the levels of p-p65, CD40 and ICAM-1 in RPMCs were significantly decreased compared with those of LPS group (0.77±0.08 vs 0.90±0.10, P相似文献