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作 者:尹文[1] 虎晓岷[1] 黄杨[1] 袁静[2] 宋祖军[1]
机构地区:[1]第四军医大学西京医院急诊科,西安710032 [2]解放军第五医院
出 处:《中国现代医学杂志》2003年第11期30-33,共4页China Journal of Modern Medicine
基 金:国家自然科学基金资助项目 ( 3 0 0 0 0 165 )
摘 要:目的 :探讨山莨菪碱 (6 5 4 - 2 )对创伤性急性肺损伤 (ALI)炎症反应影响及可能的治疗机制。方法 :采用家兔创伤性ALI模型 ,实验动物随机分为正常对照 (C)组 (8只 )、创伤模型 (M )组 (8只 )、6 5 4 - 2干预 (T)组 (8只 ) ,进行各组动物动脉血气、肺湿 /干 (U/D)比值 ,血浆和支气管肺泡灌洗液 (BALF)中肿瘤坏死因子α(TNF-α)、白细胞介素 6 (IL - 6 )含量及BALF中C3a、C5a、白蛋白含量、中性粒细胞数量的测定。用凝胶电泳迁移率改变分析法 (EMSA)检测肺泡巨噬细胞 (PAM )核提取物中核因子 -κB(NF -κB)的活性。并进行肺组织的病理学光镜检查。结果 :6 5 4 - 2治疗能明显改善创伤性ALI动物的血气 ,减少肺W/D值 ,不同程度降低外周血TNF -α、IL - 6及BALF中TNF -α、IL - 6、C3a、C5a、白蛋白含量和白细胞数量 ,明显抑制创伤组PAM中NF -κB的活性 ,减轻肺组织的损伤程度。结论 :山莨菪碱发挥抗炎和防治创伤性ALI的作用与其对NF -κB的活性和炎性介质的调节作用密切相关。Objective: To investigate effects of anisodamine(654-2) on the inflammatory reaction and their potential treatment mechanism in traumatic acute lung injury(ALI).Methods: Rabbit models of traumatic ALI were used in this study.Rabbits were randomly divided into the normal control group (group C; n=8) , ALI model group(group M;n=8) and 654-2 treatment group(group T, n=8) . We observed the effects of 654-2 on arterial blood gas, lung wet/dry(W/D) weight, contents of tumor necrosis factor-α (TNF-α) , the Interleukin 6(IL-6) in plasma and broncholveolar lavage fluid (BALF) , and contents of C 3a, C 5a, albumin, neutrophils cell counts in BALK. By electrophoretic mobility shift assay (EMSA),the NF-κB activity of nuclear protein extracted from the PAM was measured. The histological features of lung were examined by the naked eyes and light microscope.Results: 654-2 can significantly improve the blood air, reduce the W/D value , decrease the plasma level of TNF-α, IL-6 and tissue contents of TNF-α, IL-6, C 3a , C 5a , albumin , the white blood cell counts in BALF, inhibit the activation of NF-κ B in PAM significantly, and relieve the lung tissue injury in the traumatic ALI rabbits.Conclusion:654-2 could show anti-inflammatory and protective effect in traumatic ALI,which is closely ralated to the regulatory roles of 654-2 on the NF-κ B activation and pro-inflammatory factor cecretion.
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