CAJ | 학술논문

目的探讨N-乙酰基-丝氨酰-天冬氨酰-赖氨酰-脯氨酸(AcSDKP)对大鼠肺内转化生长因子(TGF)-β1、结缔组织生长因子(CTGF)表达的影响.方法将大鼠随机分为6组.每组10只.对照组大鼠支气管内灌注1.0 ml生理盐水,矽肺模型对照1组4周后处死,矽肺模型对照2组8周后处死;矽肺模型组大鼠予SiO2混悬液50 mg/ml,矽肺模型1组4周后处死,矽肺模型2组8周后处死;抗纤维化治疗组(治疗组):支气管内灌注SiO2混悬液50mg/ml,4周后给予AcSDKP 800 μg/(kg·d),至第8周处死;预防治疗组给予AcSDKP800μg(kg·d)48h后,支气管内灌注SiO2混悬液50mg/ml,8周后处死.HE染色进行形态学观察;采用免疫组织化学法检测TGF-β1与CTGF的蛋白表达;采用实时荧光定量聚合酶链反应(PCR)及反转录-聚合酶链反应(RT-PCR)法检测TGF-β1与CTGF的mRNA表达.结果治疗组TGF-β2及CTGF蛋白表达分别为0.244±0.016、0.241±0.017,明显低于矽肺模型1组和矽肺模型2组;治疗组TGF-β1 mRNA及CTGF mRNA表达水平明显低于矽肺模型1组和矽肺模型2组,差异均有统计学意义(P<0.05);预防治疗组TGF-β1和CTGF蛋白表达和mRNA表达水平明显低于矽肺模型2组,差异均有统计学意义(P<0.05).结论 AcSDKP能减轻实验性矽肺纤维化大鼠肺组织中的TGF-β1与CTGF表达水平.
목적 탐토N-을선기-사안선-천동안선-뢰안선-포안산(AcSDKP)대대서폐내전화생장인자(TGF)-β1、결체조직생장인자(CTGF)표체적영향.방법 장대서수궤분위6조.매조10지.대조조대서지기관내관주1.0 ml생리염수,석폐모형대조1조4주후처사,석폐모형대조2조8주후처사;석폐모형조대서여SiO2혼현액50 mg/ml,석폐모형1조4주후처사,석폐모형2조8주후처사;항섬유화치료조(치료조):지기관내관주SiO2혼현액50mg/ml,4주후급여AcSDKP 800 μg/(kg·d),지제8주처사;예방치료조급여AcSDKP800μg(kg·d)48h후,지기관내관주SiO2혼현액50mg/ml,8주후처사.HE염색진행형태학관찰;채용면역조직화학법검측TGF-β1여CTGF적단백표체;채용실시형광정량취합매련반응(PCR)급반전록-취합매련반응(RT-PCR)법검측TGF-β1여CTGF적mRNA표체.결과 치료조TGF-β2급CTGF단백표체분별위0.244±0.016、0.241±0.017,명현저우석폐모형1조화석폐모형2조;치료조TGF-β1 mRNA급CTGF mRNA표체수평명현저우석폐모형1조화석폐모형2조,차이균유통계학의의(P<0.05);예방치료조TGF-β1화CTGF단백표체화mRNA표체수평명현저우석폐모형2조,차이균유통계학의의(P<0.05).결론 AcSDKP능감경실험성석폐섬유화대서폐조직중적TGF-β1여CTGF표체수평.
Objective To investigate whether the effect of N-acetyl-seryl-aspartyMysyl-pmline (AcS-DKP) on transforrming growth factor beta (TGF-β1) and connective tissus growth factor (CTGF) was involved in AcSDKP's antifibrotic effect on the rats with silicosis. Methods Rats were divided into 6 groups random-ly, 10 rats in each group: Control of sihcotic model: 1.0 ml normal sodium and was killed after 4 or 8weeks; Silicotic model 1:50 mg/ml silica suspension and was killed after 4 weeks; Silicotic model 2:50 mg/ml silica suspension and was killed after 8 weeks; Anti-fibrosis treatment of AeSDKP: after each rat was intratracheally instilled with 50 mg/ml silica suspension for 4 weeks, AcSDKP 800 μg/(kg·d) was administered into every rat and rats were killed at the 8 weeks; Preventing fibrosis treatment of AcSDKP: after AcSDKP [800 μg/(kg·d)] was administered into every rat for 48 hours, each rat was intratracheally instilled with 50 mg/ml silica suspen-sion and rats were killed at the 8 weeks. Lung fibrosis in morphology was observed by HE staining. The expres-sions of TGF-β1 and CTGF in lung were observed by immunohistochemistry. The mRNA expressions of TGF-β1and CTGF in lung were observed by real-time PCR. Results In anti-fibrosis treatment of AcSDKP group, protein expression of TGF-β1 and CTGF were (0.244±0.016) and (0.241±0.017)respectively, and significant-ly lower that those in the silicotic model 1 and 2 groups; mRNA expressions of TGF-β1, and CTGF decreased, mRNA expressions of CTGF were significantly lower that those in the silicotic model l and 2 groups(P<0.05) ; In preventing fibrosis treatment of AcSDKP group, protein expression and mRNA expression of TGF-β1 were signifieandy lower that those in the silicotic model 2 group (P<0.05). Conclusion AcSDKP can decrease the expressions of TGF-β1 and CTGF in lung tissues of the rats with experimentally induced pulmonary fibrosis.