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肺纤维化大鼠肺泡Ⅱ型细胞中细胞因子的表达
引用本文:宋明臣,何冰,邱忠民. 肺纤维化大鼠肺泡Ⅱ型细胞中细胞因子的表达[J]. 中华结核和呼吸杂志, 1998, 21(4): 221-223
作者姓名:宋明臣  何冰  邱忠民
作者单位:北京医科大学第一医院呼吸内科
摘    要:目的观察博莱霉素致肺纤维化大鼠肺泡I型上皮细胞肿瘤坏死因子(TNFα)和血小板衍化生长因子(PDGF)表达的变化。方法大鼠气管内灌注博莱霉素A5复制肺纤维化模型,分别于注药后第3、7、14和28天处死动物,进行免疫组织化学染色;同时提取肺泡Ⅱ型上皮细胞总RNA进行Northern杂交。结果正常大鼠肺泡Ⅱ型上皮细胞不表达TNFα和PDGF;而肺纤维化大鼠肺泡Ⅱ型上皮细胞则表达TNFα和PDGF。其中TNFα表达高峰在注药后第28天;PDGF的表达高峰在注药后第7天。结论肺纤维化大鼠肺泡Ⅱ型细胞过度表达TNFα和PDGF,参与了肺纤维的发病过程。

关 键 词:肺纤维化  肺泡Ⅱ型上皮细胞  肿瘤坏死因子  血小板衍化生长因子  博莱霉素

Expressions of TNF alpha, PDGF in alveolar type II epithelial cells of rats with bleomycin-induced pulmonary fibrosis]
II. Expressions of TNF alpha, PDGF in alveolar type II epithelial cells of rats with bleomycin-induced pulmonary fibrosis][J]. Chinese journal of tuberculosis and respiratory diseases, 1998, 21(4): 221-223
Authors:II
Affiliation:Division of Respiratory Medicine, First Hospital of Beijign Medical University, Beijing 100034.
Abstract:OBJECTIVE: The expressions of TNF alpha and PDGF in alveolar type II epithelial cells of rats with bleomycin(BLM)-induced pulmonary fibrosis were studied. METHOD: A single intratracheal injection of BLM was administrated to induce pulmonary fibrosis of rats. Animals were killed at day 3,7,14 and 28 after BLM-administration. The immunohistochemical methods were used to analyze the expressions of TNF alpha and PDGF proteins in alveolar epithelium of rats. The total RNA was extracted from the alveolar type II epithelial cells of rats and the expressions of TNF alpha and PDGF mRNA were analyzed with Northern blot. RESULT: TNF alpha and PDGF were expressed in the alveolar type II epithelial cells of BLM-administrated rats. The expression of TNF alpha elevated in median and late-stage of the process and reached the peak at day 28. While the expression of PDGF elevated in early-stage and reached the peak at day 7. By contrast, TNF alpha and PDGF weren't expressed in the alveolar type II epithelial cells of normal controls. CONCLUSION: The results show that the alveolar type II epithelial cell from rats with pulmonary fibrosis overexpresses TNF alpha and PDGF and they may play roles in the pathogenesis of lung fibrosis.
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