CAJ | 학술논문

目的初步探讨氨基胍(aminoguanidine,AG)在博莱霉素(bleomycin,BLM)诱导的大鼠肺纤维化模型中的作用及其机制.方法实验第1天将48只SD大鼠随机分为8组:正常对照组、BLM模型组、AG干预组及AG对照组(包括低、中、高3个剂量组),每组6只,经气道滴入BLM/生理盐水后,于实验第2天开始按低、中、高3个剂量给予AG,2周后处死所有大鼠,收集标本.利用Masson染色,观察肺组织纤维化的情况,并进行纤维化评分;利用碱性水解法测定肺组织中羟脯氨酸的含量;利用RT-PCR的方法测定肺组织中热休克蛋白47的基因表达.结果 AG干预组与BLM模型组相比较,前者的纤维化程度均有所减轻,且呈现出剂量依赖性,尤其在中、高剂量组,纤维化评分、羟脯氨酸含量、热休克蛋白47的基因表达出现明显下降(P值均＜0.01).AG对照组与正常对照组比较差异无统计学意义.结论 AG能有效降低BLM诱导的肺纤维化程度,其机制可能与下调热休克蛋白47等纤维化因子的表达有关.
목적 초보탐토안기고(aminoguanidine,AG)재박래매소(bleomycin,BLM)유도적대서폐섬유화모형중적작용급기궤제.방법 실험제1천장48지SD대서수궤분위8조:정상대조조、BLM모형조、AG간예조급AG대조조(포괄저、중、고3개제량조),매조6지,경기도적입BLM/생리염수후,우실험제2천개시안저、중、고3개제량급여AG,2주후처사소유대서,수집표본.이용Masson염색,관찰폐조직섬유화적정황,병진행섬유화평분;이용감성수해법측정폐조직중간포안산적함량;이용RT-PCR적방법측정폐조직중열휴극단백47적기인표체.결과 AG간예조여BLM모형조상비교,전자적섬유화정도균유소감경,차정현출제량의뢰성,우기재중、고제량조,섬유화평분、간포안산함량、열휴극단백47적기인표체출현명현하강(P치균＜0.01).AG대조조여정상대조조비교차이무통계학의의.결론 AG능유효강저BLM유도적폐섬유화정도,기궤제가능여하조열휴극단백47등섬유화인자적표체유관.
Objective To determine the effects of aminoguanidine(AG) in murine bleomycin(BLM)induced lung fibrosis. Methods Forty-eight rats were randomly divided into 8 groups (6 rats in each group),including normal control group, BLM group,and three different doses of AG groups with their corresponding AG control groups. One day after administration of bleomycin intratracheally, aminoguanidine was given orally in each AG group once daily,according to the dosage designed. Total rats were killed two weeks later,and lung tissues were collected and frozen for examinations. Masson trichrome stain was used for Ashcroft score to estimate the degree of lung fibrosis; contents of hydroxyproline were measured by the method of alkaline hydrolization,and the expression of heat shock protein 47 (HSP47) was determined by RT-PCR.Results The degree of fibrosis dose-dependently decreased in the bleomycin groups treated with AG compared with BLM group,especially in the moderate and high dose AG-treated groups ( P＜0.01) ,as well as the contents of lung hydroxyproline and expression of HSP47 mRNA in lung tissues. No statistic difference was found between normal control group and AG control group. Conclusions AG significantly attenuates BLM-induced lung fibrosis,and it may relate to the downregulation of HSP47 expression.