论文部分内容阅读
本研究观察了雾化吸入氨基胍(aminoguanidine,AG)对博莱霉素(bleomycin,BLM)所致肺纤维化大鼠肺内结缔组织生长因子(connective tissuegrowth factor,CTGF)上调的影响。大鼠气管内一次性滴注BLM复制肺纤维化动物模型,以气管内滴注等容积的生理盐水(normal saline,NS)作对照。在气管滴注BLM后第1天至第30天期间,给大鼠雾化吸入AG(2mmol/L、10mmol/L或50mmol/L,5min/次,一天两次),以雾化吸入NS作对照。采用硝酸还原法、氯胺-T法、Masson染色法、Western blot和RT-PCR分别检测出肺血浆NO2-/NO3-含量(代表NO含量)、肺羟脯氨酸含量、肺胶原纤维含量以及肺CTGF蛋白和mRNA含量。结果显示:气管滴注BLM后第14天大鼠出肺血浆中NO2-/NO3-含量、气管滴注BLM后第30天大鼠的肺羟脯氨酸含量、肺胶原纤维含量、肺CTGF蛋白和mRNA水平均高于相应的对照组大鼠(均P<0.01);上述指标均在雾化吸入10mmol/L和50mmol/L AG后有所改善(出肺血浆中NO2-/NO3-含量P<0.01,其余均P<0.05)。以上结果表明,AG能有效地防止肺纤维化大鼠肺内CTGF的上调,这可能是其防止肺纤维化形成的作用机制之一。
This study investigated the effects of aminoguanidine (AG) on the up-regulation of connective tissue growth factor (CTGF) in lungs of pulmonary fibrosis rats induced by bleomycin (BLM). The rats were intratracheally instilled with BLM to make the model of pulmonary fibrosis. The normal saline (NS) was intratracheally instilled. Rats were nebulised with AG (2mmol / L, 10mmol / L or 50mmol / L, 5min / time twice a day) during the first day to the 30th day after tracheal instillation of BLM, Control. Pulmonary plasma NO2- / NO3- content (representing NO content), lung hydroxyproline content, lung collagen fiber content were detected by nitrate reduction, chloramine-T method, Masson staining, Western blot and RT- Lung CTGF protein and mRNA content. The results showed that the level of NO2- / NO3- in the lungs of the rats excreted on the 14th day after intratracheal intratracheal intratracheal intratracheal intratracheal instillation, the content of lung hydroxyproline, the content of lung collagen fibers, the level of lung CTGF protein (All P <0.01). The above indexes were all improved after inhalation of 10 mmol / L and 50 mmol / L AG (NO2- / NO3- content in the plasma of the lung <0.01, the rest were P <0.05). The above results indicate that AG can effectively prevent the up-regulation of CTGF in the lung of rats with pulmonary fibrosis, which may be one of the mechanisms of preventing the formation of pulmonary fibrosis.