摘要
目的观察重组人Ⅱ型肿瘤坏死因子受体-抗体融合蛋白（rhTNFR—Fc，益赛普）对博来霉素（BLM）-A5所致肺间质病变大鼠转化生长因子（TGF）-β1表达的影响。方法SD雄性大鼠45只，随机分为对照组、模型组和rhTNFR—Fc治疗组（治疗组），每组15只。各组动物于第7、14、28天随机处死5只，取肺组织进行苏木素-伊红（HE）和Masson染色，用免疫组织化学法检测肺组织TGF-β1的表达水平。结果对照组未见明显胶原沉积、炎症及纤维化改变，治疗组各时期肺泡炎和肺纤维化程度均较模型组轻，差异有统计学意义（P〈0．01）。模型组各时期TGF—β1的表达较对照组增加，差异有统计学意义（P〈0．01）；治疗组第7、14天TGF—β1的表达较对照组增加，差异有统计学意义（P〈0．01），第28天稍高于对照组，但差异无统计学意义（P〉0．05）。治疗组第7天比模型组减低，差异有统计学意义（P〈0．05），第14、28天比模型组减低差异有统计学意义（P〈0．01）。结论rhTNFR—Fc能减轻BLM—A5诱导的大鼠肺泡炎和肺纤维化，可能与抑制肺组织TGF—β1表达有关。
Objective To observe the effect of recombinant human tumor necrosis factor receptor-Fc fusion protein （rhTNFR-Fc, etanercept） on the expression of transforming growth factor-β1 （TGF-β1） in bleomycin induced interstitial lung disease of rats. Methods Forty-five male Sprague-Dawley （SD） rats were randomly divided into three groups （control group, model group and rhTNFR-Fc treatment group, 15 rats in each）, on the 7th, 14th and 28th days, five rats of each group were killed. The lungs were incised to make pathological sections which were stained with HE and Masson, and the expression of TGF-β1 was detected by immunohistochemical technique. Results There was no collagen deposition, alveolitis and fibrosis changes in the control group. The alveolitis and fibrosis of the treatment group was less severe than that in the model group （P〈0.01）. The expression of TGF-β1 in the model group was significantly higher than that in the control group （P〈0.01）. In the 7th and 14th days, the expression of TGF-β1 in the treatment group was significantly higher than that in the control group （P〈0.01）. Although that in the 28th day was a slightly higher but no statistical significance （P〉0.05） could be detected. In the treatment group, the expression of TGF-β1 was lower in the 7th day （P〉0.05） and was significantly lower in the 14th and 28th days than that in the model group （P〈0.01）. Conclusion Recombinant human tumor necrosis factor receptor-Fc fusion protein can alleviate the severity of alveolitis and pulmonary fibrosis induced by Bleomycin-A5 in rats, which may be due to the inhibition of TGF-β1 overexpression.
出处
《中华风湿病学杂志》
CAS
CSCD
2008年第11期754-756,I0002,共4页
Chinese Journal of Rheumatology
关键词
肺疾病
间质性
博来霉素
受体
肿瘤坏死因子
Ⅱ型
转化生长因子Β1
Lung disease, interstitial
Bleomycin
Receptor, tumor necrosis factor, type Ⅱ
Transforming growth factor beta
