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Dynamic Expression of Tumor Necrosis Factor-α and Vascular Endothelial Growth Factor in Rat Model of Pulmonary Emphysema Induced by Smoke Exposure
In order to explore the roles of tumor necrosis factor-α (TNF-α) and vascular endothelial growth factor (VEGF) in the pathogenesis of pulmonary emphysema, male Wistar rats were randomized into group At, group A2.5 and group A4, each with smoke exposure for 1 month, 2.5 months or 4 months, respective...
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Published in: | Journal of Huazhong University of Science and Technology. Medical sciences 2007-10, Vol.27 (5), p.505-507 |
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Main Author: | |
Format: | Article |
Language: | English |
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Online Access: | Get full text |
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Summary: | In order to explore the roles of tumor necrosis factor-α (TNF-α) and vascular endothelial growth factor (VEGF) in the pathogenesis of pulmonary emphysema, male Wistar rats were randomized into group At, group A2.5 and group A4, each with smoke exposure for 1 month, 2.5 months or 4 months, respectively. Group B t, group B2.5 and group B4 were used as non smoking controls at corresponding time points. TNF-α in bronchoalveolar lavage fluid (BALF) and expression of VEGF in lung tissue was determined by ELISA or by SABC immunohistochemistry assay either. Lung slices were stained with hematoxylin and eosin (HE). Results showed that in animal with smoke exposure the mean linear interceptor (Lm), an index of pulmonary emphysema and the content of TNF-α in BALF increased gradually, on contrary, the expression of VEGF in lung tissue decreased (P〈0.05). This phenomenon was not obvious in animals without smoke exposure. Lm was negatively correlated to the VEGF expression (7=--0.81, P〈0.01) and positively correlated to TNF-α concentration (7 = 0.52, P〈0.004), which implies that smoke exposure decreased the expression of VEGF and increased the expression of TNF-α. It is plausible to speculate that the imbalance of TNF-α and VEGF may play an important role in the pathogenesis of smoke-induced pulmonary emphysema. |
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ISSN: | 1672-0733 1993-1352 |
DOI: | 10.1007/s11596-007-0507-1 |