抗转化生长因子β1（TGFβ1）单克隆抗体和抗血管内皮生长因子（VEGF）单克隆抗体可抑制硝酸银诱导的实验性胸膜固定术。
Monoclonal antibodies anti-TGFβ1 and anti-VEGF inhibit the experimental pleurodesis induced by silver nitrate.
作者信息
Marchi Evaldo, Vargas Francisco S, Takemura Renan L, Acencio Milena M, Antonangelo Leila, Teixeira Lisete R, Light Richard W
机构信息
University of São Paulo Medical School, Pulmonology, Al. das Castanheiras, 196, Terras de São Carlos, Jundiai 13216-770, Brazil.
出版信息
Growth Factors. 2012 Oct;30(5):304-9. doi: 10.3109/08977194.2012.721359.
BACKGROUND
The mechanisms underlying pleural inflammation and pleurodesis are poorly understood. We hypothesized that the cytokines transforming growth factor β (TGFβ1) and vascular endothelial growth factor (VEGF) play a major role in pleurodesis after intrapleural silver nitrate (SN) injection.
METHOD
Forty rabbits received intrapleurally 0.5% SN alone or 0.5% SN + anti-TGFβ1, anti-IL-8, or anti-VEGF. After 28 days, the animals were euthanized and macroscopic pleural adhesions, microscopic pleural fibrosis, and collagen deposition were analyzed for characterization of the degree of pleurodesis (scores 0-4).
RESULTS
Scores of pleural adhesions, pleural fibrosis, total collagen, and thin collagen fibers deposition after 28 days were significantly lower for 0.5% SN + anti-TGFβ1 and 0.5% SN + anti-VEGF. Significant correlations were found between macroscopic adhesion and microscopic pleural fibrosis with total collagen and thin collagen fibers.
CONCLUSIONS
We conclude that both TGFβ1 and VEGF, but not IL-8, mediate the pleural inflammatory response and pleurodesis induced by SN.
背景
胸膜炎症和胸膜固定术的潜在机制尚不清楚。我们假设细胞因子转化生长因子β（TGFβ1）和血管内皮生长因子（VEGF）在胸膜内注射硝酸银（SN）后的胸膜固定术中起主要作用。
方法
40只兔子接受胸膜内单独注射0.5% SN或0.5% SN + 抗TGFβ1、抗IL - 8或抗VEGF。28天后，对动物实施安乐死，并分析宏观胸膜粘连、微观胸膜纤维化和胶原沉积情况，以确定胸膜固定术的程度（评分0 - 4）。
结果
28天后，0.5% SN + 抗TGFβ1组和0.5% SN + 抗VEGF组的胸膜粘连、胸膜纤维化、总胶原和细胶原纤维沉积评分显著降低。宏观粘连与微观胸膜纤维化之间以及总胶原和细胶原纤维之间存在显著相关性。
结论
我们得出结论，TGFβ1和VEGF而非IL - 8介导了SN诱导的胸膜炎症反应和胸膜固定术。
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