大鼠放射性肺纤维化病理过程的形态计量学研究

为阐明放射性肺纤维化的病变规律和发生机理提供形态依据，应用图像分析技术，对放射性肺纤维化形成过程中肺间质、肺泡腔、肺内基质弹力纤维含量、肺内肥大细胞嗜碱性颗粒含量及肺内成纤维细胞胶原ｍＲＮＡ含量进行了定量测定。结果显示，随照射时间延长，肺泡壁渐增厚、肺间质所占面积增大，肺泡腔进行性缩小。弹力纤维于照后１个月时即见增多持续至６个月，而于照射后９－１２个月近于正常。肥大细胞嗜碱性颗粒含量于照射１、２个月明显减少，３－９个月恢复近正常水平。肺内成纤维细胞胶原ｍＲＮＡ含量于照射后每个时间点均有不同程度增加。表明放射性肺纤维化病变是个动态发展过程；肺内肥大细胞可能参与了纤维化的形成；肺内胶原的转录增强可能是放射性肺纤维化形成的关键步骤之一。     

PKC基因在人肺癌中的转录表达

目的 探讨ＰＫＣ－β１基因转录表达与肺癌临床病理生理特征的关系。方法 应用Ｎｏｒｔｈｅｒｎ印迹杂交方法检测５０例肺癌组织、癌旁肺组织、远癌肺组织和３０例肺良性病变组织ＰＫＣ－β１ ｍＲＮＡ表达水平。结果 （１）肺癌组织中ＰＫＣ－β１ ｍＲＮＡ表达水平显著高于癌旁肺组织,远癌肺组织和肺良性病变肺组织（Ｐ〈０．０１）;（２）低分化肺癌中ＰＫＣ－β１表达水平显著高于中－高分化肺癌（Ｐ〈０．０５）;（３）     

肺腺癌及鳞癌MDR1-mRNA和MRP-mRNA表达的研究

观察３０例肺癌组织及癌肺组织ＭＤＲ１－ｍＲＮＡ及ＭＲＰ－ｍＲＮＡ的表达。方法：ＲＴ－ＰＣＲ方法。结果：ＭＤＲ１－ｍＲＮＡ在肺癌组织及癌旁肺组织的表达阳性率分别为４０．０％及１６．６７％（Ｐ＝０．０４５）,ＭＤＲ１－ｍＲＮＡ的表达与细胞分化程度,临床分期及病理类型无关;ＭＲＰ－ｍＲＮＡ在肺癌主癌旁肺组织的表达分别为４３．３３％及２６．６７％,ＭＲＰ＝ｍＲＮＡ的表达与细胞分化程度有关,低分者ＭＲＰ的表     

ＤＮＡ结合抑制因子１在非小细胞肺癌组织中的表达

目的　探讨ＤＮＡ结合抑制因子１（Ｉｄ１）在非小细胞肺癌（ＮＳＣＬＣ）发生、发展中的作用及与ＮＳＣＬＣ临床病理特征之间的联系。方法　选取３０例ＮＳＣＬＣ癌组织、癌旁组织和正常肺组织以及１０例肺良性病变组织和正常肺组织,采用ＲＴ-ＰＣＲ和免疫组化ＳＰ法测定其Ｉｄ１ｍＲＮＡ和Ｉｄ１蛋白的表达情况。结果　（１）Ｉｄ１ｍＲＮＡ、Ｉｄ１蛋白在ＮＳＣＬＣ癌组织中的阳性表达率为９６.６７％（２９／３０）、９３.３３％（２８／３０）,在癌旁组织中的阳性表达率为１３.３３％（４／３０）、１０％（３／３０）,在ＮＳＣＬＣ正常肺组织、肺良性病变组织及其正常肺组织中均未见表达。（２）ＮＳＣＬＣ癌组织Ｉｄ１ｍＲＮＡ和Ｉｄ１蛋白的表达强度随癌细胞分化程度的降低而增强。（３）ＮＳＣＬＣ患者Ｉｄ１ｍＲＮＡ和Ｉｄ１蛋白的表达与病理类型、瘤体大小、淋巴结转移及预后无明显相关性。结论　Ｉｄ１因子可能是鉴别ＮＳＣＬＣ与肺良性病变的重要分子标记物之一,且其表达水平与ＮＳＣＬＣ癌细胞分化程度呈负相关。     

肺癌组织中Ⅰ型胶原纤维mRNA的原位杂交观察

目的：讨论Ⅰ型胶原纤维的增生与肺癌发生发展的关系。方法：采用基因原位杂交的方法对４０例肺癌和正常肺组织中Ⅰ型胶原ｍＲＮＡ的表达进行了研究。结果：肺癌组织中Ⅰ型胶原纤维的合成明显强于肺组织。Ⅰ型胶原ｍＲＮＡ阳性的成纤维细胞分布于癌巢周边和癌巢内。结论：Ⅰ型胶原纤维的增生在肺癌的发生发展中起一定作用。     

卡铂复合液对大鼠腹腔内化疗后腹膜Ⅰ型和Ⅲ型腾的mRNA表达的影响

为探讨含有透明质酸钠和白蛋的卡铂复合液对腹腔内化疗后腹粘连的抑制，采用斑点杂交和原位杂交方法观察其对大鼠腹腔内化疗后腹膜组织Ⅰ型和Ⅲ型胶原ｍＲＮＡ水平的影响。研究表明卡铂复合液腹腔内化疗 对胶原基因表达的增加有明显抑制作用，可明显地减少成纤维细胞胶原合成和抑制腹腔粘连形成。     

Annexin Ⅰ在α粒子转化细胞及肺癌组织中高表达

目的：探讨Ａｎｎｅｘｉｎ　Ⅰ表达与肺癌及细胞转化的关系。方法：Ｗｅｓｔｅｒｎ印迹、Ｎｏｒｔｈｅｒｎ印迹检测永生化 人支气管上皮 ＢＥＰ２Ｄ细胞及α粒子照射转化后 ＢＥＰ２Ｄ细胞中 Ａｎｎｅｘｎｉ　Ⅰ在 ｍＲＮＡ和蛋白质水平的表达,细胞免疫 化学检测 Ａｎｎｅｘｉｎ　Ⅰ在 ＢＥＰ２Ｄ细胞中的分布。Ｗｅｓｔｅｒｎ印迹检测肺癌病人正常组织与肿瘤组织中 Ａｎｎｅｘｉｎ　Ⅰ蛋白质的 表达。结果： Ａｎｎｅｘｉｎ　Ⅰ在α粒子照射转化后 ＢＥＰ２Ｄ细胞中 ｍＲＮＡ和蛋白质水平上的表达光密度均为永生化人支气 管上皮 ＢＥＰ２Ｄ细胞的 １.５倍; Ａｎｎｅｘｉｎ　Ⅰ在 ＢＥＰ２Ｄ细胞中分布于胞浆及细胞膜。本研究收集了 ８例肺鳞癌、４例肺腺 癌病人的肺肿瘤组织及正常组织,Ａｎｎｅｘｉｎ　Ⅰ在肺癌组织中的表达明显高于正常组织（Ｐ＜０.０１）,Ａｎｎｅｘｉｎ　Ⅰ在肿瘤 组织中表达的光密度与正常肺组织之比为 ２．７。结论： Ａｎｎｅｘｉｎ　Ⅰ在肺癌组织过表达,表明 Ａｎｎｅｘｉｎ　Ⅰ可能与肺癌及 细胞恶性转化的发生发展有关。永生化及α粒子照射恶转 ＢＥＰ２Ｄ细胞为进一步研究 Ａｎｎｅｘｉｎ　Ⅰ在恶性转化中的作 用提供了良好的模型。     

CYPIAI mRNA在大鼠脑内的分布以及溴氰菊酯对其影响的研究

目的：研究ＣＹＰ１Ａ１ ｍＲＮＡ在大鼠脑内的分布以及溴氰菊酯对其影响。方法：采用ＲＴ－ＰＣＲ及ｃＲＮ ｄｏｔ ｂｌｏｔ方法检测大鼠不同脑区ＣＹＰ１Ａ１ ｍＲＮＡ的表达。结果：大鼠脑区ＣＹＰ１Ａ１ ｍＲＮＡ分布不致,在所检测的脑区中,下丘脑量丰富,其次是皮层、小脑;在溴氰菊酯１／１０ＬＤ５０（１２．５ｍｇ．ｋｇ＾－１．ｄ＾－１）腹腔注射连续５ｄ的作用下,溴氰菊酯对大鼠脑内ＣＹＰ１Ａ１ ｍＲＮＡ有明显的抑制作用,并以皮层和下丘脑为基。结论：ＣＹＰ１Ａ１ ｍＲＮＡ在大鼠脑内的分布不一致,溴氰菊酯抑制脑内ＣＰＹ１Ａ１ ｍＲＮＡ的表达。     

人肺癌组织细胞Na^＋／H^＋交换蛋白—1基因的表达与其抗凋亡的 …

目的：通过对临床人肺癌组织Ｎａ＾＋／Ｈ＾＋交换蛋白－１（ＮＨＥ－１）ｍＲＮＡ的表达的检测，探讨肿瘤治疗新的特异靶点。方法：采用ＲＮＡ原位分子杂交法（ＲＮＡ－ＩＭＨ）检测了２７例人肺癌组织和正常肺组织ＮＨＥ－１ｍＲＡＮ的表达。结果：人肺癌组织细胞ＮＨＥ－１ｍＲＮＡ的表达显著增强，呈过表达，而各病理类型音我显著差异。结论：人肺癌组织细胞中ＮＨＥ－１ＭＲＮＡ过表达这一区别于正常组织细胞的分子生物学特征与     

人胃癌细胞株ＳＧＣ-７９０１体外乏氧环境ＨＩＦ-１α、ＶＥＧＦ-Ａ和ＶＥＧＦ-Ｄ基因表达变化

目的：观察乏氧干预对人胃癌细胞ＳＧＣ-７９０１乏氧诱导因子-１α（ＨＩＦ-１α）、血管内皮生长因子-Ａ（ＶＥＧＦ-Ａ）和血管内皮生长因子 Ｄ（ＶＥＧＦ-Ｄ）表达的影响,以及乏氧诱导因子-１α和血管内皮生长因子表达的相关性。方法：将人胃癌细胞ＳＧＣ-７９０１体外培养并乏氧干预０、４、１６、２４ｈ,以反转录 聚合酶链式反应（ＲＴ-ＰＣＲ）方法检测４组ＨＩＦ-１α、ＶＥＧＦ-Ａ、ＶＥＧＦ-ＤｍＲＮＡ的表达情况;免疫印迹（Ｗｅｓｔｅｒｎｂｌｏｔ）检测４组ＨＩＦ-１α、ＶＥＧＦ-Ａ、ＶＥＧＦ-Ｄ蛋白表达情况。结果：与０ｈ相比,４ｈＨＩＦ-１αｍＲＮＡ转录处于下降水平（Ｐ＜０.０５）,１６ｈＨＩＦ-１αｍＲＮＡ转录上升（Ｐ＜０.０５）,２４ｈ转录达到最高水平（Ｐ＜０.０５）。ＶＥＧＦ-ＡｍＲＮＡ和ＶＥＧＦ-ＤｍＲＮＡ表达量均随时间的延长逐渐增加（Ｐ＜０.５）。ＨＩＦ-１α、ＶＥＧＦ-Ａ、ＶＥＧＦ-Ｄ蛋白表达量随乏氧时间的延长逐渐增加（Ｐ＜０.０５）。结论：胃癌细胞株ＳＧＣ-７９０１乏氧环境中,ＨＩＦ-１α、ＶＥＧＦ-Ａ和ＶＥＧＦ-Ｄ的ｍＲＮＡ与蛋白表达均明显增加。     

Radiation-induced hypoxia may perpetuate late normal tissue injury.

PURPOSE: The purpose of this study was to determine whether or not hypoxia develops in rat lung tissue after radiation. METHODS AND MATERIALS: Fisher-344 rats were irradiated to the right hemithorax using a single dose of 28 Gy. Pulmonary function was assessed by measuring the changes in respiratory rate every 2 weeks, for 6 months after irradiation. The hypoxia marker was administered 3 h before euthanasia. The tissues were harvested at 6 weeks and 6 months after irradiation and processed for immunohistochemistry. RESULTS: A moderate hypoxia was detected in the rat lungs at 6 weeks after irradiation, before the onset of functional or histopathologic changes. The more severe hypoxia, that developed at the later time points (6 months) after irradiation, was associated with a significant increase in macrophage activity, collagen deposition, lung fibrosis, and elevation in the respiratory rate. Immunohistochemistry studies revealed an increase in TGF-beta, VEGF, and CD-31 endothelial cell marker, suggesting a hypoxia-mediated activation of the profibrinogenic and proangiogenic pathways. CONCLUSION: A new paradigm of radiation-induced lung injury should consider postradiation hypoxia to be an important contributing factor mediating a continuous production of a number of inflammatory and fibrogenic cytokines.     

应用基因表达谱芯片筛选高能X射线诱导HFL-1细胞胶原相关基因

目的 探讨高能X射线对人胚肺成纤维细胞(HFL-1)细胞胶原表达产生影响,并筛选胶原相关基因,为临床放射性肺纤维化的治疗提供理论依据。方法 将体外培养的HFL-1细胞随机分为对照组和放射组,放射组细胞予6 MV X射线5 Gy单次照射。照射后24 h以消化法检测两组细胞羟脯氨酸(HYP)表达情况,RT-PCR及蛋白印迹法检测Ⅰ、Ⅲ型胶原基因及蛋白表达情况,采用基因芯片技术分析基因表达谱改变情况。结果 照射后24 h放射组细胞HYP表达显著高于对照组(1.834μg/ml∶4.912 μg/ml,P=0.000)。放射组照射后24 h Ⅰ、Ⅲ型胶原基因及蛋白表达均明显高于对照组(18.535∶186.779,P=0.000;4.337∶24.425,P=0.000)。两组细胞差异表达的基因为1879个,其中放射组上调基因771个、下调基因为1108个。参与纤维化的基因上调5倍以上的有TGF-β₁、TGF-β₃、MMP28、MMP26、MMP27和SMAD6。     

X-rays modulate extracellular matrix in vivo.

X-rays have an antiangiogenic effect in the chicken embryo chorioallantoic membrane (CAM) model of in vivo angiogenesis. Our study demonstrates that X-rays induce an early apoptosis of CAM cells, modulate the synthesis and deposition of extracellular matrix (ECM) proteins involved in regulating angiogenesis and affect angiogenesis induced by tumour cells implanted onto the CAM. Apoptosis was evident within 1-2 hr, but not later than 6 hr after irradiation. Fibronectin, laminin, collagen type I, integrin alpha(v)beta3 and MMP-2 protein amounts were all decreased 6 hr after irradiation. In contrast, collagen type IV, which is restricted to basement membrane, was not affected by irradiation of the CAM. There was a similar decrease of gene expression for fibronectin, laminin, collagen type I and MMP-2, 6 hr after irradiation. The levels of mRNA for integrin alpha(v)beta3 and collagen type IV were unaffected up to 24 hr after irradiation. The decrease in both protein and mRNA levels was reversed at later time points and 48 hr after irradiation, there was a significant increase in the expression of all the genes studied. When C6 glioma tumour cells were implanted on irradiated CAMs, there was a significant increase in the angiogenesis induced by tumour cells, compared to that in non-irradiated CAMs. Therefore, although X-rays have an initial inhibitory effect on angiogenesis, their action on the ECM enhances new vessel formation induced by glioma cells implanted on the tissue.     

Comparison of single,fractionated and hyperfractionated irradiation on the development of normal tissue damage in rat lung

The effect of fractionated thoracic irradiation on the development of normal tissue damage in rats was compared to that produced by single doses. Animals received a single dose of 15 Gy, 30 Gy in 10 daily fractions of 3 Gy each (fractionation), or 30 Gy in 30 fractions of 1 Gy each 3 times a day (hyperfractionation). The treatments produced minimal lethality since a total of only 6 animals died between days 273 and 475 after the initiation of treatment, with no difference in survival observed between the control and any of the 3 treated groups. Despite the lack of lethality, evidence of lung damage was obtained by histological examination. At times less than 180 days after treatment, the lungs of animals receiving a single dose of 15 Gy displayed more severe changes than did animals from either fractionation group. At longer times after treatment (days 261 and 475), the histological appearances within each group were changed, collagen deposits and fibrosis being the most significant observations. Animals that had received either single doses or fractionated doses had more of the pulmonary parenchyma involved than did animals that had received hyperfractionated doses. We conclude that, in the rat lung model, a total radiation dose of 30 Gy fractionated over 14 days produces no more acute lethality nor damage to lung tissue than does 15 Gy delivered as a single dose. However, long-term effects as evidenced by deposits of collagen and development of fibrosis are significantly reduced by hyperfractionation when compared to single doses and daily fractionation.     

大鼠心脏组织TGF-β1 mRNA表达水平与放射性损伤关系的实验研究

背景与目的:放射性心脏损伤是影响接受纵隔放疗患者长期生存的预后因素之一,本研究探讨大鼠受照后心脏转化生长因子β1(transforming growth factorβ1,TGF-β1)mRNA水平随时间的变化及与放射性损伤发生发展的关系,为进一步抗纤维化药物治疗放射性心脏损伤的实验研究提供参考。方法:将60只大鼠分为两组。对照组大鼠不接受照射,受照组给予心脏照射20Gy,分别在受照后第1天、第2、4、8、12、24周每组解剖5只大鼠,检测血清肌钙蛋白和肌酸激酶同工酶(isoenzyme of creatine kinase,CK-MB)水平的变化,定量PCR检测心脏组织TGF-β1mRNA表达,并行心脏组织学切片评价心脏受照后损伤程度。结果:照射后24h实验组血清肌钙蛋白即有升高,2周时达到高峰[(0.73±0.11)ng/mL],与对照组[(0.11±0.04)ng/mL]相比差异有统计学意义(P<0.05);实验组CK-MB无明显变化,两组相比差异无统计学意义(P>0.05)。心脏TGF-β1mRNA表达在照射后第1天即出现升高,并在第2、12周出现高峰[受照组为(8.55±1.19)×10-8μg/mL以及(4.63±0.41)×10-8μg/mL,对照组为(1.27±0.11)×10-8μg/mL以及(1.35±0.15)×10-8μg/mL],两组相比差异有统计学意义(P<0.05)。心脏受照后自第2周起纤维细胞比例增加[受照组为(2.87±0.37)%,对照组为(1.14±0.55)%],随时间延长放射性损伤逐渐加重,两组相比差异有统计学意义(P<0.05);心肌组织纤维化程度的变化与TGF-β1mRNA表达水平的变化有显著的正相关性(P<0.05,r=0.48)。结论:TGF-β1参与心肌纤维化的形成。在TGF-β1分泌高峰期使用抗纤维化药物对其水平进行抑制,可能对组织纤维化形成产生预防作用。     

X射线对肺癌细胞系p57kip2转录表达的影响

目的:研究X射线对肺癌细胞系NCI-H226和A549的印记基因p57kip2转录表达的影响。方法:对数生长期的肺癌细胞系NCI-H226和A549,分别予以2、4、8和12GyX射线照射,并于照射前和照射后6、12、24、36和48h分别提取RNA,采用RT-PCR技术检测各时相p57kip2mRNA的含量,分析不同剂量X射线照射后对其转录水平的影响。结果:两组肺癌细胞p57的转录表达在不同照射剂量和不同时间水平间差异有统计学意义,P<0·05,A549经过X射线照射后,p57kip2的mRNA含量明显升高,且与照射剂量呈线性依赖关系;NCI-H226虽然未见明显规律,但在X射线照射后的峰值mR-NA含量均明显升高。结论:X射线照射后能够上调肺癌细胞p57kip2的mRNA的表达,预示着p57可能参与了放射线所致细胞周期重新分布和细胞凋亡的过程,并且可能预测肺癌细胞的放射敏感性,但其表达与时间剂量的关系尚需要进一步研究。     

NF-κB及下游通路与大鼠急性期放射性心肌纤维化相关性研究

目的 建立急性放射性心脏损伤大鼠模型,观察急性心肌组织炎症反应和纤维化等病理学表现,探讨NF-κB及其下游通路是否与心肌纤维化相关。方法 成年雄性SD大鼠14只,完全随机法均分为对照组和照射组。照射组采用6 MV X线单次20 Gy经心前区照射构建放射性心脏损伤模型,照射后第14天应用HE染色观察心肌细胞及细胞间质形态学改变;Masson染色观察胶原纤维分布情况,并以CVF作半定量分析指标进行成组t检验。蛋白印记法及qPCR法分别检测大鼠心肌组织NF-κB基团成员p50、p65及其下游通路HIF-1α、CTGF、COL-1蛋白及mRNA表达量变化。结果 大鼠心脏局部照射后第14天,照射组较对照组心肌细胞水肿明显、排列紊乱,部分心肌细胞断裂、心肌细胞核轻度固缩、核染色加深,少量异形细胞核,心肌间质可见大量炎症细胞浸润、成纤维细胞增多。Masson染色显示胶原纤维广泛分布于心肌细胞间质,与对照组相比照射组大鼠心肌胶原明显增多,正常心肌细胞排列紊乱、有被胶原纤维替代的趋势。半定量分析结果显示照射组CVF明显高于对照组(22.05%:3.76%,P=0.003)。蛋白印记法及qPCR法结果显示心肌组织p50、p65、HIF-1α、CTGF、 COL-1蛋白表达及mRNA水平照射组较对照组均明显升高(P均<0.05)。结论 急性放射性心脏损伤病理学表现为心肌细胞水肿、细胞间质大量炎症细胞浸润、成纤维细胞增多、胶原纤维增多。其损伤机制可能与心肌组织NF-κB激活有关,同时放射线可引起其下游通路HIF-1α、CTGF在蛋白和基因水平表达上调,可能在放射性心肌炎症向纤维化发展过程中起到重要作用。     

Degradation of basement membrane type IV collagen and lung subendothelial matrix by rat mammary adenocarcinoma cell clones of differing metastatic potentials

A series of rat 13762NF mammary adenocarcinoma cell clones and subclones of various lung metastatic potentials were examined for their abilities to degrade rat lung subendothelial matrix and purified basement membrane type IV collagen. Metastatic potentials were simultaneously determined based on the ability to form "spontaneous" lung metastases after s.c. injection or "experimental" lung metastases after i.v. injection of cells. Microvessel endothelial cells isolated from rat lung were grown in vitro, and the subendothelial matrix containing type IV collagen was metabolically labeled with [3H]proline. When mammary adenocarcinoma cells were placed on the isolated subendothelial matrix, fragmentation and solubilization of [3H]proline-labeled components were observed; highly metastatic 13762NF cells solubilized the matrix at higher rates than did poorly metastatic cells. The 13762NF cells were assayed for type IV collagenolytic activity using [3H]proline-labeled type IV collagen purified from Engelbreth-Holm-Swarm tumor as a substrate. We found excellent correlation between the type IV collagenolytic activities of living cells and their "spontaneous" lung metastatic potentials (r = 0.993). The levels of type IV collagenolytic activity in the conditioned medium depended on the cell culture conditions. In the presence or absence of acid-treated fetal bovine serum, highly metastatic cells secreted higher amounts of type IV collagenolytic enzymes in active and latent forms than did poorly metastatic cells. Incubation of procollagen type IV with medium conditioned by highly metastatic 13762NF cells and treated with trypsin resulted in the production of several large fragments characteristic of type IV collagen. The results suggest that enzymatic degradation of basement membrane type IV collagen is important in lung metastasis of 13762NF mammary adenocarcinoma cells.     

益气活血中药对放射损伤大鼠肺组织TGF-β1和Ⅰ、Ⅲ型胶原合成的影响

目的：观察小剂量重复照射下不同时相大鼠肺组织转化生长因子-β1（TGF-β1）的表达和Ⅰ、Ⅲ型胶原纤维的动态变化,以及益气活血中药干预的影响,探讨益气活血中药防治放射性肺损伤的作用及机理。方法：96只Wistar种雌性大鼠随机分为照射加中药组（A组）30只、照射加氨溴索组（B组）30只、单纯照射组（C组）30只、正常对照组（D组）6只。用直线加速器对前3组大鼠右肺进行分次照射（5Gy/次,1次/w,累积剂量为30Gy）,于照射开始后第4、6、8、12、26w5个时间点分别处死3组大鼠各6只,取肺组织切片行TGF-β1和Ⅰ、Ⅲ型胶原纤维免疫组化检测,观察各组大鼠肺组织不同时相TGF-β1的表达和胶原纤维含量的改变。结果：单纯照射组大鼠肺组织TGF-β1于照射第4w增高,第12w达到高峰;胶原纤维合成在第4w开始,第12w明显增快,至26w达到高峰。中药干预组各时相大鼠肺组织TGF-β1表达及Ⅰ、Ⅲ型胶原纤维增生程度均明显低于单纯照射组（P〈0.05）;各时相值与照射加氨溴索组近似,相比无统计学差异（P〉0.05）。结论：在小剂量重复照射过程中,组织TGF-β1表达与组织胶原纤维合成有明显的同步性,而早期应用益气活血中药可抑制TGF-β1的表达,并减轻早期放射性肺炎的炎症反应和后期放射性肺纤维化的程度,因而对放射性肺损伤具有防治作用。