BACKGROUND: Urinary trypsin inhibitor (UTI) inhibits the inflammatory response and protects against ischemia-reperfusion (I/R) injury. The inflammatory response is mediated by nuclear factor-kappa B (NF-kappa B) and i...BACKGROUND: Urinary trypsin inhibitor (UTI) inhibits the inflammatory response and protects against ischemia-reperfusion (I/R) injury. The inflammatory response is mediated by nuclear factor-kappa B (NF-kappa B) and its related target genes and products such as vascular endothelial cell adhesion molecule and CXC chemokines. We aimed to assess the roles of those mediators in a UTI-treated mouse model of hepatic I/R injury. METHODS: Treatment group 1 (UTI given 5 minutes prior to liver ischemia), treatment group 2 (UTI given 5 minutes after the anhepatic phase) and a control group were investigated. Blood and liver samples were obtained and compared at 1, 3, 6 and 24 hours after reperfusion. RESULTS: Attenuation of pathological hepatocellular damage was greater in the treatment groups than in the control group (P < 0.05). Compared with the control group, the UTI treatment groups showed significantly lower serum alanine aminotransferase and aspartate aminotransferase levels, decreased myeloperoxidase activity, and reduced NF-kappa B activation. Also downregulated was the expression of tumor necrosis factor-alpha, cytokine-induced neutrophil chemoattractant, and macrophage inflammatory protein-2 at the mRNA level. P-selectin protein and intercellular adhesion molecule-1 protein expression were also downregulated. In addition, the treatment group I showed a better protective effect against I/R injury than the treatment group 2. CONCLUSIONS: UTI reduces NF-kappa B activation and downregulates the expression of its related mediators, followed by the inhibition of neutrophil aggregation and infiltration in hepatic I/R injury. The protective role of UTI is more effective in prevention than in treatment.展开更多
目的研究在呼吸机所致肺损伤(VILI)的炎症反应中加用呼气末正压(PEEP)对核因子-κB(NF-κB)的活性变化的影响。方法健康成年新西兰白兔30只随机分为3组:PEEP组(致伤通气+3 cm H2O PEEP)、ZEEP组(致伤通气+0 cm H2O PEEP组)和对照组(始...目的研究在呼吸机所致肺损伤(VILI)的炎症反应中加用呼气末正压(PEEP)对核因子-κB(NF-κB)的活性变化的影响。方法健康成年新西兰白兔30只随机分为3组:PEEP组(致伤通气+3 cm H2O PEEP)、ZEEP组(致伤通气+0 cm H2O PEEP组)和对照组(始终以正常条件通气)。机械通气开始后4 h处死动物。采用Western-blot法检测家兔肺组织NF-κB及核因子抑制蛋白(IκB-α)的含量。结果家兔在致伤通气4 h后,肺组织NF-κB表达显著增加,而在致伤通气的同时加用PEEP,肺组织NF-κB表达明显减少。结论在机械通气过程中加用PEEP可通过减少NF-κB的表达保护肺组织减轻损伤。展开更多
目的:探讨围产期缺血缺氧对新生大鼠肺超微结构和肿瘤坏死因子α(TNFα-)及核因子κB抑制蛋白(κI-Bα)表达的影响。方法:结扎孕鼠一侧子宫角血管(另一侧宫内胎鼠作为对照),建立围产期缺血缺氧动物模型。电镜下观察肺组织超微结构变化...目的:探讨围产期缺血缺氧对新生大鼠肺超微结构和肿瘤坏死因子α(TNFα-)及核因子κB抑制蛋白(κI-Bα)表达的影响。方法:结扎孕鼠一侧子宫角血管(另一侧宫内胎鼠作为对照),建立围产期缺血缺氧动物模型。电镜下观察肺组织超微结构变化并分别采用ELISA、RT-PCR和W estern b lot杂交法观察不同程度缺血缺氧新生大鼠肺组织TNFα-蛋白和mRNA及I-κBα表达的变化。结果:宫内急性缺血缺氧20 m in时,新生大鼠Ⅱ型肺泡上皮细胞和毛细血管内皮细胞受损;肺组织TNFα-蛋白和mRNA表达明显增强(P均<0.01),κI-Bα表达明显减弱(P<0.05),并随缺血缺氧时间延长病变加重。结论:围产期急性缺血缺氧致新生大鼠肺损伤,Iκ-Bα和TNFα-的异常表达可能是肺损伤的重要原因。展开更多
文摘BACKGROUND: Urinary trypsin inhibitor (UTI) inhibits the inflammatory response and protects against ischemia-reperfusion (I/R) injury. The inflammatory response is mediated by nuclear factor-kappa B (NF-kappa B) and its related target genes and products such as vascular endothelial cell adhesion molecule and CXC chemokines. We aimed to assess the roles of those mediators in a UTI-treated mouse model of hepatic I/R injury. METHODS: Treatment group 1 (UTI given 5 minutes prior to liver ischemia), treatment group 2 (UTI given 5 minutes after the anhepatic phase) and a control group were investigated. Blood and liver samples were obtained and compared at 1, 3, 6 and 24 hours after reperfusion. RESULTS: Attenuation of pathological hepatocellular damage was greater in the treatment groups than in the control group (P < 0.05). Compared with the control group, the UTI treatment groups showed significantly lower serum alanine aminotransferase and aspartate aminotransferase levels, decreased myeloperoxidase activity, and reduced NF-kappa B activation. Also downregulated was the expression of tumor necrosis factor-alpha, cytokine-induced neutrophil chemoattractant, and macrophage inflammatory protein-2 at the mRNA level. P-selectin protein and intercellular adhesion molecule-1 protein expression were also downregulated. In addition, the treatment group I showed a better protective effect against I/R injury than the treatment group 2. CONCLUSIONS: UTI reduces NF-kappa B activation and downregulates the expression of its related mediators, followed by the inhibition of neutrophil aggregation and infiltration in hepatic I/R injury. The protective role of UTI is more effective in prevention than in treatment.
文摘目的研究在呼吸机所致肺损伤(VILI)的炎症反应中加用呼气末正压(PEEP)对核因子-κB(NF-κB)的活性变化的影响。方法健康成年新西兰白兔30只随机分为3组:PEEP组(致伤通气+3 cm H2O PEEP)、ZEEP组(致伤通气+0 cm H2O PEEP组)和对照组(始终以正常条件通气)。机械通气开始后4 h处死动物。采用Western-blot法检测家兔肺组织NF-κB及核因子抑制蛋白(IκB-α)的含量。结果家兔在致伤通气4 h后,肺组织NF-κB表达显著增加,而在致伤通气的同时加用PEEP,肺组织NF-κB表达明显减少。结论在机械通气过程中加用PEEP可通过减少NF-κB的表达保护肺组织减轻损伤。
文摘目的:探讨围产期缺血缺氧对新生大鼠肺超微结构和肿瘤坏死因子α(TNFα-)及核因子κB抑制蛋白(κI-Bα)表达的影响。方法:结扎孕鼠一侧子宫角血管(另一侧宫内胎鼠作为对照),建立围产期缺血缺氧动物模型。电镜下观察肺组织超微结构变化并分别采用ELISA、RT-PCR和W estern b lot杂交法观察不同程度缺血缺氧新生大鼠肺组织TNFα-蛋白和mRNA及I-κBα表达的变化。结果:宫内急性缺血缺氧20 m in时,新生大鼠Ⅱ型肺泡上皮细胞和毛细血管内皮细胞受损;肺组织TNFα-蛋白和mRNA表达明显增强(P均<0.01),κI-Bα表达明显减弱(P<0.05),并随缺血缺氧时间延长病变加重。结论:围产期急性缺血缺氧致新生大鼠肺损伤,Iκ-Bα和TNFα-的异常表达可能是肺损伤的重要原因。
