CAJ | 학술논문

目的探讨放射性肺炎方(ARPD)干预放射性肺纤维化的作用机制.方法将105只雄性SD大鼠采用随机数字表法分为中药(6MV X射线,15 Gy单次照射+ARPD,10 ml·kg-1·d-1)组、单纯照射组(6MVX射线,15 Gy单次照射)和对照组,每组35只,分别于第15、30、60、75、90、105、140天各收集5只大鼠肺组织及血液样本,肺组织行常规病理学检查；Western blot 及RT-PCR法检测转化生长因子-β1(TGF-β1)、纤溶酶原激活物抑制因子-1(PAI-1)、Ⅲ型胶原(collagen typeⅢ,CⅢ)蛋白及基因在组织中的动态表达；ELISA法检测血清TGF-β1及血浆PAI-1含量；酸水解法及碱水解法分别检测组织及血清羟脯氨酸(HYP).结果受照肺组织病理学检查在各时间点均见炎性反应改变,60 d后出现纤维化,中药组早期炎性反应、后期纤维化均显著轻于单纯照射组.中药组30 d后TGF-β1、PAI-1、CⅢ蛋白及基因在肺组织中表达水平低于同期单纯照射组(蛋白:t =2.49 ～3.74,t=2.63 ～4.57,t=2.76～3.83；基因:t=2.59～4.33,t=2.83 ～4.62,t=2.83～3.96,P＜0.05),15d后血浆PAI-1、血清TGF-β1水平低于同期单纯照射组(t=2.85～6.27,t=3.69 ～ 5.27,P＜0.05),60 d后肺组织及血清HYP水平低于同期单纯照射组(t=3.65 ～4.40,t=6.56 ～ 3.75,P＜0.05),且肺组织TGF-β1分别与PAI-1及CⅢ的蛋白(r=0.604、0.759,P＜0.05)和基因(r=0.519、0.816,P＜0.05)变化水平呈显著正相关.结论 ARPD可通过下调TGF-β1、PAI-1,减少CⅢ的合成干预放射性肺纤维化.
목적 탐토방사성폐염방(ARPD)간예방사성폐섬유화적작용궤제.방법 장105지웅성SD대서채용수궤수자표법분위중약(6MV X사선,15 Gy단차조사+ARPD,10 ml·kg-1·d-1)조、단순조사조(6MVX사선,15 Gy단차조사)화대조조,매조35지,분별우제15、30、60、75、90、105、140천각수집5지대서폐조직급혈액양본,폐조직행상규병이학검사；Western blot 급RT-PCR법검측전화생장인자-β1(TGF-β1)、섬용매원격활물억제인자-1(PAI-1)、Ⅲ형효원(collagen typeⅢ,CⅢ)단백급기인재조직중적동태표체；ELISA법검측혈청TGF-β1급혈장PAI-1함량；산수해법급감수해법분별검측조직급혈청간포안산(HYP).결과 수조폐조직병이학검사재각시간점균견염성반응개변,60 d후출현섬유화,중약조조기염성반응、후기섬유화균현저경우단순조사조.중약조30 d후TGF-β1、PAI-1、CⅢ단백급기인재폐조직중표체수평저우동기단순조사조(단백:t =2.49 ～3.74,t=2.63 ～4.57,t=2.76～3.83；기인:t=2.59～4.33,t=2.83 ～4.62,t=2.83～3.96,P＜0.05),15d후혈장PAI-1、혈청TGF-β1수평저우동기단순조사조(t=2.85～6.27,t=3.69 ～ 5.27,P＜0.05),60 d후폐조직급혈청HYP수평저우동기단순조사조(t=3.65 ～4.40,t=6.56 ～ 3.75,P＜0.05),차폐조직TGF-β1분별여PAI-1급CⅢ적단백(r=0.604、0.759,P＜0.05)화기인(r=0.519、0.816,P＜0.05)변화수평정현저정상관.결론 ARPD가통과하조TGF-β1、PAI-1,감소CⅢ적합성간예방사성폐섬유화.
Objective To investigate the therapeutic effects and mechanism of anti-radiation pneumonia decoction(ARPD) on radiation induced lung fibrosis in rats.Methods One hundred and five male SD rats in a SPF grade were divided into Chinese medicine group,single radiation group and control group by random digits table method,with 35 in each group.After anesthetization,rats in Chinese medicine and single radiation groups were exposed to 6 MV X-rays at the dose of 15Gy.Rats in Chinese medicine group were treated with ARPD at the dosage of 10 ml·kg-1 ·d-1 once a day,but rats in single radiation group did not receive ARPD treatment.Rats in control group were treated with neither irradiation nor drugs.Five rats of each group were killed and the lung tissues and blood samples were collected at 15,30,60,75,90,105 and 140 d.The pathological changes of lung tissues were observed and the tissue protein and gene expressions of TGF-β1,PAI-1 and collagen type Ⅲ(C Ⅲ) were assayed by Western blot and RT-PCR.ELISA was used to detect serum TGF-β1 and plasma PAI-1.Tissue and serum HYP were determined by acid hydrolysis and alkaline hydrolysis methods respectively.Results Inflammation was found in the lung tissues of all the exposed rats.Obvious pathological lung fibrosis was found at 60 d,the inflammation and the fibrosis in treated group were slighter than those in single radiation group.In Chinese medicine group,the protein and gene expression levels of TGF-β1,PAI-1,C Ⅲ 30 d(Protein:t =2.49-3.74,t =2.63-4.57 and t =2.76-3.83;Gene:t =2.59-4.33,t =2.83-4.62 and t =2.83-3.96,P＜0.05),serum TGF-β1 and plasma PAI-1 15 dlater (t =2.85-6.27 and t =3.69-5.27,P＜0.05),and the levels of tissue and serum HYP60 dlater (t=3.65-4.40 and t =6.56-3.75,P＜0.05),all of them were lower than those in single radiation groups.There were significant positive correlations between tissue TGF-β1 and PAI-1 as well as C Ⅲ (Protein expression:r =0.604,0.759,P ＜0.05;Gene expression:r=0.519,0.816,P＜0.05).Conclusions ARPD may inhibit the pulmonary fibrosis by decreasing the levels of TGF-β1,PAI-1 and C Ⅲ.