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作 者:郭红[1,2] 陈晓玲[1] 陈超[3] 金辉[4] 艾洁[1]
机构地区:[1]河北医科大学基础医学研究所病理生理研究室,河北石家庄050017 [2]唐山工人医院呼吸内科,河北唐山063000 [3]河北医科大学基础医学研究所药理研究室,河北石家庄050017 [4]河北医科大学基础医学研究所临床学院实验中心,河北石家庄050017
出 处:《中国应用生理学杂志》2009年第4期543-547,I0013,共6页Chinese Journal of Applied Physiology
基 金:国家自然科学基金(30570789);河北省自然科学基金资助项目(C2004000582)
摘 要:目的:观察雾化吸入氨基胍(AG)对博莱霉素(BLM)诱导的肺纤维化的防治作用,并探讨其可能的机制。方法:60只雄性SD大鼠,随机分为以下4组:博莱霉素+生理盐水(BLM+NS)组、博莱霉素+AG低剂量组(BLM+10mmol/L AG组)、博莱霉素+AG高剂量组(BLM+50 mmol/L AG组)和生理盐水+生理盐水组(NS+NS组)。气管内一次性滴注BLM(5 mg/kg)或等体积NS的当天,给大鼠雾化吸入生理盐水(NS),10 mmol/L AG或50 mmol/L AG,每次5 min,每日2次,持续30 d。检测肺动脉血NO2-/NO3-含量、肺组织羟脯氨酸含量、肺组织病理学变化和肺动脉血中脂质过氧化物(LPO)含量。结果:与对照大鼠相比,气管内滴注BLM后第14 d,肺动脉血NO2-/NO3-含量明显增高(P<0.01),气管内滴注BLM后第30 d,大鼠的肺组织羟脯氨酸含量增高(P<0.05),肺泡炎分级增加(P<0.01),肺动脉血中LPO含量增高(P<0.01)。上述指标均在雾化吸入10 mmol/L和50 mmol/L AG后有所改善(P<0.01,P<0.05,P<0.05,P<0.01)。结论:雾化吸入AG对BLM诱发的肺纤维化有防治作用;此作用与其阻止肺内氧化损伤有关。Aira: To explore the effects of aminoguanidine(AG) inhalation on bleomycin (BLM)-induced fibrosis in lungs of rats and its possible mechanism. Methods: Sixty male Sprague-Dawley rats were randomly divided into 4 groups: BLM plus normal saline (NS) group, BLM plus 10 mmoL/L AG group, BLM plus 50 mmol/L AG group, and NS plus NS group. At the same day when administrated by single intratracheal instillation of BLM(5 mg/kg) or equal volume of NS as control, the rats received NS (the same volume as AG) or AG inhalation( 10 mmol/L AG, or 50 mmol/L AG, 5 min/each time,2/day) for 30 d. The nitrite/nitrate(NO2^-/NO3^-) content of plasma in pulmonary artery, hydroxyproline content and the pathological changes in lungs, as well as lipid peroxide(LPO) content of plasma in pulmonary artery were examined. Results: The NO2^-/NO3^- content of plasma in pulmonary artery was increased in rats on day 14 after intratracheal instillation of BLM, compared with that of the control rats( P 〈 0.01). The hydroxyproline content in lung, the grade of pulmonary alveolitis and the content of LPO of plasma in pulmonary artery were increased in rats on day 30 after intratracheal instillation of BLM, compared with that of the control rats, respectively( P 〈 0.05, P 〈 0.01, P 〈 0.01). The above-mentioned changes were ameliorated by AG inhalation ( 10 mmol/L AG, or 50 mmol/ LAG, 5 min/each time,2/day) for 30 d ( P 〈 0.01, P 〈 0.05, P 〈 0.05, P 〈 0.01). Conclusion: AG inhalation has anti-action on BLM-induced fibrosis in lung, which might be related to blockage of oxidative injury in lung.
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