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目的通过观察结核性胸膜炎患者单个核细胞 DNA 氧化损伤程度、总抗氧化能力及抗氧化剂褪黑素对其的作用,评价褪黑素对结核性胸膜炎患者胸水单个核细胞 DNA 损伤的体外修复作用。方法用单细胞凝胶电泳检测25例健康人外周血、28例结核性胸膜炎患者胸水和外周血单个核细胞 DNA 损伤(以彗星率表示),及经褪黑素处理的20例结核性胸膜炎患者胸水单个核细胞DNA 损伤。用菲罗啉比色法检测健康人血浆、结核性胸膜炎患者胸水和血浆总抗氧化能力。结果健康人外周血单个核细胞彗星率为(8.9±3.7)%,血浆总抗氧化能力为(10.61±1.39)U/ml。结核性胸膜炎患者胸水单个核细胞彗星率为(41.3±14.5)%,高于其外周血[(21.2±4.2)%,P<0.01];胸水总抗氧化能力为(5.17±1.19)U/ml,低于其血浆[(8.66±1.59)U/ml,P<0.01]。经10 μmol/L褪黑素体外作用4 h 后,胸水单个核细胞彗星率由(40.8±9.3)%降至(11.0±3.7)%(t=15.251,P<0.01)。胸水单个核细胞彗星率与总抗氧化能力呈负相关(r=-0.425,P<0.05)。结论结核性胸膜炎患者存在 DNA 氧化损伤、氧化/抗氧化失衡,病变局部较全身明显。体外经褪黑素处理,能促进结核性胸膜炎患者胸水单个核细胞 DNA 损伤的修复,可能与其抗氧化作用有关。
OBJECTIVE: To evaluate the effect of melatonin on the DNA damage of pleural fluid mononuclear cells in patients with tuberculous pleurisy by observing the degree of DNA oxidative damage, the total antioxidant capacity and the effect of the antioxidant melatonin on it in patients with tuberculous pleurisy. Methods The DNA damage of pleural fluid and peripheral blood mononuclear cells in 25 healthy volunteers and 28 patients with tuberculous pleurisy were detected by single cell gel electrophoresis (in terms of comet rate), and 20 patients with tuberculous pleurisy treated with melatonin Pleural effusion mononuclear cells DNA damage. Phenanthroline colorimetry was used to detect the total anti-oxidative capacity of pleural effusion and plasma in healthy human plasma and tuberculous pleurisy. Results The comet rate of peripheral blood mononuclear cells was (8.9 ± 3.7)% and the total plasma antioxidant capacity was (10.61 ± 1.39) U / ml. The comet rate of pleural effusion mononuclear cells in tuberculous pleurisy patients was (41.3 ± 14.5)%, higher than that in peripheral blood [(21.2 ± 4.2)%, P <0.01]. The total antioxidant capacity of pleural effusion was (5.17 ± 1.19) U / ml , Lower than that of plasma [(8.66 ± 1.59) U / ml, P <0.01]. After treated with 10 μmol / L melatonin in vitro for 4 h, the comet rate of pleural effusion mononuclear cells decreased from (40.8 ± 9.3)% to (11.0 ± 3.7)% (t = 15.251, P <0.01). Pleural fluid mononuclear cell comet rate and total antioxidant capacity was negatively correlated (r = -0.425, P <0.05). Conclusion There is DNA oxidative damage, oxidative / anti-oxidative imbalance in patients with tuberculous pleurisy, and the local lesion is more obvious than the whole body. In vitro melatonin treatment can promote the repair of DNA damage in pleural fluid mononuclear cells in patients with tuberculous pleurisy, which may be related to its anti-oxidative effects.