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氨基胍对博莱霉素致大鼠肺纤维化的干预作用及机制

Intervention of aminoguandine on bleomycin-induced pulmonary fibrosis in rats and its mechanisms
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摘要 目的探讨氨基胍(AG)对博莱霉素(BLM)诱导SD大鼠肺纤维化中的干预作用。方法将116只SD大鼠随机分成5组:正常对照组、BLM组、AG组、激素组和AG+激素组。经气道给予BLM或生理盐水后,每天给不同组别相应的药物或生理盐水连续28 d。分别在第7,14,21,28天随机处死各组老鼠5只。处死前,取肺泡灌洗液用硝酸还原酶法测一氧化氮(NO)的表达。用碱水解法测肺组织中羟脯氨酸的含量及用RTPCR检测肺组织中转化生长因子(TGF)-β1 mRNA的相对表达量。结果①与BLM组比较,AG组、激素组和AG+激素组支气管肺泡灌洗液(BALF)中NO的表达在第7,14天下降(P<0.05),肺组织羟脯氨酸含量减少(P<0.05)。②各治疗组肺组织TGF-β1 mRNA的相对表达量和BLM组比较在7,14,21 d明显增加(P<0.05)。结论 AG可以降低BLM诱导的肺纤维化程度,作用机制可能是通过抑制TGF-β1的基因表达。 Objective To investigate aminoguandine ( AG)′s role in bleomycin ( BLM)-induced pulmonary fibrosis in rats .Methods One hundred and sixteen rats were randomly divided into 5 groups, including normal control, BLM, AG, dexamethasone group, AG+dex-amethasone groups .After administration of BLM intratracheally , AG, dexamethasone were given in each group daily , according to the dosage designed.Rats were killed on the 7th, 14th, 21th, 28th days.The content of NO in the bronchoalveolar lavage fluid (BALF) was meas-ured.The degree of fibrosis was evaluated by pulmonary hydroxyproline assay , the expression of TGF-β1 mRNA in lung tissues by RT-PCR. Results (1)The expressions of NO in BALF in AG, dexamethasone, AG+dexamethasone groups were lower than those in BLM group on the 7th,14th days(P<0.05).The expressions of hydroxyproline in lung tissues were lower than those in BLM group on the 14th, 21th days (P<0.05).(2)The expressions of TGF-β1 mRNA in lung tissues were lower than those in BLM group on the 7th, 14th, 21th days(P<0.05 ) .Conclusions AG attenuates BLM-induced lung fibrosis , and it may be relate to the downregulation of TGF-β1 expression .
出处 《中国老年学杂志》 CAS CSCD 北大核心 2014年第8期2199-2201,共3页 Chinese Journal of Gerontology
基金 卫生部科研项目(WKJ2006-2-026) 上海市自然科学基金项目(10ZR1422600)
关键词 氨基胍 肺纤维化 一氧化氮 转化生长因子Β1 Aminoguandine Pulmonary Fibrosis Nitric oxide Transforming growth factor β1
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