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胸腔内注入四环素引起炎性反应,损伤胸膜间皮细胞,使胸膜下结缔组织增厚,造成胸膜脏层与壁层粘连。可用以治疗反复胸水。然而其发生机制及临床疗效不同(40%~60%)的原因,至今不明。最近发现,胸水中的原膜降解金属蛋白酶(MMP)可降解初级Ⅳ型胶原和明胶,溶解胸膜损伤后的粘连和纤维化,促进胸膜腔的完整。其活性依赖于分子中心Zn~(++)的存在。四环素是一种金属螯合物,可有效抑制MMP。本文研究了四环素抑制胸水中MMP活性及抑制人纤维肉瘤合成MMP的剂量,已知纤维肉瘤细胞产生MMP的量类似于胸水。
Intrathoracic injection of tetracycline cause inflammatory reactions, damage to the pleural mesothelial cells, pleural connective tissue thickening, resulting in adhesion of visceral visceral and parietal pleura. Can be used to treat repeated pleural effusion. However, its mechanism of occurrence and clinical efficacy of different (40% to 60%) of the reasons, so far unknown. Recently, it was found that degradation of primary collagen type IV (MMP) in pleural effusion degrades primary collagen type IV and gelatin, dissolves adhesions and fibrosis after pleural injury, and promotes the integrity of the pleural cavity. Its activity depends on the existence of molecular center Zn ~ (++). Tetracycline is a metal chelate that effectively inhibits MMPs. In this paper, tetracycline inhibition of pleural fluid MMP activity and inhibition of human fibrosarcoma synthesis of MMP dose, known fibrosarcoma cells produce MMP similar to pleural effusion.