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作 者:刘建明[1] 廖前德[2] 唐文祥[1] 孙圣华[1] 刘备战[1] 刘新民[3]
机构地区:[1]中南大学湘雅三医院呼吸科,湖南长沙410013 [2]中南大学湘雅医院 [3]中南大学公共卫生学院,湖南长沙410078
出 处:《南方医科大学学报》2012年第4期548-552,共5页Journal of Southern Medical University
基 金:湖南省自然科学基金(06SK4060);湖南省卫生厅科研基金(B2007082)
摘 要:目的研究肿瘤坏死因子-α(TNF-α)对慢性阻塞性肺疾病(COPD)模型鼠的营养状态和呼吸肌蛋白质分解代谢率的影响。方法将90只健康Wistar大鼠随机分为模型组(A)70只,对照组(B)20只。采用气管内注入猪胰弹性蛋白酶、熏香烟和限制营养的方法建立COPD鼠模型和COPD营养不良鼠模型。模型制作成功后,将A组分为COPD营养正常组(A1),COPD营养不良组(A2)和COPD营养不良干预组(A3)。A3组采用尾静脉注射TNF-αMcAb 0.1 mg/kg,进行干预。酶联免疫吸附法测定大鼠血清、呼吸肌匀浆中TNF-α含量,自动生化仪测定血浆葡萄糖、白蛋白、甘油三酯含量,反相高效液相色谱荧光法测定呼吸肌中三甲基组氨酸(3-MH)、酪氨酸(Tyr)含量。结果 1:A2组血清和呼吸肌匀浆TNF-α含量和血浆葡萄糖、甘油三酯明显高于B、A1和A3组(P<0.01);A2组膈肌重量,白蛋白含量明显低于B、A1和A3组(P<0.01);2:A2组呼吸肌匀浆中3-MH、Tyr含量均明显高于B、A1和A3组(P<0.01);3:A2组呼吸肌TNF-α含量与3-MH、Tyr含量呈明显正相关(R=0.866,P<0.01;R=0.883,P<0.01),TNF-αMcAb干预后,蛋白质分解代谢率降低。结论 TNF-α是引起COPD鼠发生营养不良和呼吸肌蛋白质分解代谢率增高的因素之一。Objective To investigate the effect of tumor necrosis factor-α(TNF-α) on nutritional status and proteolysis of respiratory muscle in a rat model of chronic obstructive pulmonary disease(COPD).Methods Ninety healthy male adult Wistar rats were randomly divided into model group(A) and normal control group(B).COPD malnutrition rat models were established by cigarettes smoke and nutrient limitation and divided into normal nutrition COPD group(A1),malnutrition COPD group(A2),and malnutrition COPD intervention group(A3).In group A3,the rats received intravenous injection of TNF-α mAb(0.1 mg/kg).TNF-α levels in the serum and respiratory muscle homogenates were measured using enzyme-linked immunosorbent assay(ELISA),and plasma levels of glucose,albumin,and triglyceride were measured with an automatic biochemisty analyzer.High-performance liquid chromatography was used to measure the contents of 3-methylhistidine and tyrosine in the respiratory muscle homogenates.Results The serum TNF-α level and plasma levels of glucose and triglyceride were significantly higher but the plasma albumin level was significantly lower in group A2 than in groups B,A1,and A3(P0.01).The contents of 3-MH and Tyr in the respiratory muscle homogenates were significantly higher in group A2 than in the other 3 groups(P0.01,P0.01).TNF-α in the respiratory muscle showed a strong positive correlation to 3-MH and Tyr.Conclusion TNF-α is one of the causes of increased proteolysis of the respiratory muscle.
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