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作 者:蒋一茵[1] 钱燕[2] 胡良冈[3] 孟卫霞[2] 吴步猛[4]
机构地区:[1]舟山市人民医院儿科,316004 [2]温州医学院附属第一医院新生儿科,325000 [3]温州医学院病理生理学科,325000 [4]温州医学院动物房,325000
出 处:《中国小儿急救医学》2008年第5期458-461,共4页Chinese Pediatric Emergency Medicine
摘 要:目的探讨丹参提取物764.3对高氧暴露所致新生大鼠急性肺损伤的保护作用,并将其作用与超氧化物歧化酶(SOD)进行比较。方法采用新生spragueDawley大鼠置于≥90% O2中7d以建立高氧急性肺损伤模型,分别用SOD和764—3进行干预,对比肺系数、丙二醛(MDA)含量、SOD活性、辐射状肺泡计数(RAC)和病理形态学变化,并采用脱氧核糖核酸转移酶介导的细胞凋亡标记技术法(TUNEL)检测肺细胞凋亡情况。结果SOD干预组和764.3干预组在高氧暴露7d时的MDA含量和凋亡细胞数均低于高氧对照组(P〈0.05或P〈0.01),病理形态学改变要轻于高氧对照组,RAC及SOD活性则要高于高氧对照组(P〈0.05或P〈0.01),且两种抗氧化剂作用近似(P〉0.05)。但764—3干预组的肺水肿与高氧对照组差异无显著性(P〉0.05)。结论764—3对新生大鼠高氧所致的急性肺损伤有一定的保护作用。Objective To study the protective effect of Radix Salviae Milliorrhizae Extract (764-3) on hyperoxia-induced acute lung injury of neonatal rats and to compare the effect of it with that of superoxide dismutase (SOD). Methods Hyperoxic lung injury model was established by putting Sprague Dawley neonatal rats into self-made oxygen box within high-concentration oxygen(≥90 % O2)for 7 days. Interfered with SOD and 764-3 respectively, the lung index, contents of malondialdehyde (MDA), activity of SOD, radical alveolar counts (RAC) and pathological changes have been compared. Meanwhile, terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) was utilized to detect the number of apoptosis of lung ceils. Results On the seventh day, the contents of MDA and the number of apoptosis of lung cells of SOD prevention group and 764-3 prevention group were lower than those of the hyperoxia-exposed group ( P 〈 0.05 or P 〈 0.01 ), while RAC and activity of SOD were higher(P 〈 0.05 or P 〈 0.01 ) ; pathological changes of apoptosis of lung cells of SOD prevention group and 764-3 prevention group were leas than those of the hyperoxia-exposed group, The protective effect of SOD and 764-3 were similar(P 〉 0.05 ). However, compared with those of hyperoxia-exposed group, the lung index of 764-3 prevention group showed insignificant difference(P 〉 0.05). Conclusion Radix Salviae Milliorrhizae Extract (764-3) may have certain protective effect on hyperoxia-indueed acute lung injury.
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