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对２０例哮喘发作患者和２１例健康对照者血中丙二醛（ＭＤＡ）含量，抗氧化酶包括趋氧化物歧化酶（ＳＯＤ）、过氧化氢酶（ＣＡＴ）、谷胱甘肽过氧化物酶（ＧＳＨ─Ｐｘ）活性及ＴＸＡ２、ＰＧＩ２各自的稳定代谢产物ＴＸＢ２、６─Ｋｅｔｏ─ＰＧＦ１α水平进行了测定。结果：（１）哮喘发作组ＭＤＡ含量（８．１６±１．５８ｎｍｏｌ／ｍｌ）较对照组（６．０８±１．３９ｎｍｏｌ／ｍｌ）显著增高（ｐ＜０．００１），而ＳＯＤ、ＣＡＴ、ＧＳＨ─Ｐｘ活性均显著降低（ｐ分别小于０．００５、０．００１和０．０５），说明哮喘患者脂质对氧化反应增强，抗氧化能力低下，在其发病中起重要作用。（２）哮喘发作组血清ＭＤＡ含量与ＳＯＤ活性呈显著的直线负相关（ｒ＝－０．４８１，ｐ＜０．０２５），提示哮喘患者抗氧化能力低下可能是脂质过氧化反应增强的原因。（３）与对照组相比，哮喘发作组ＴＸＢ２水平及ＴＡＢ２／６─Ｋｅｔｏ─ＰＧＦ１α增高，６─Ｋｅｔｏ─ＰＧＦ１α水平降低，差异均有显著性，表明ＴＸＡ２─ＰＧＩ２失衡参与了哮喘的发病。（４）哮喘发作组血清ＭＤＡ含量与血浆ＴＸＢ２水平呈直线正相关（ｒ＝０．６３７，Ｐ＜０．００２５），与６─Ｋｅｔｏ─ＰＧＦ１α水平呈直线负?
The levels of malondialdehyde (MDA) in blood of 20 asthmatic patients and 21 healthy controls were measured. Antioxidant enzymes including oxidase (SOD), catalase (CAT), glutathione peroxidase Enzyme (GSH-Px) activity and TXA2, PGI2 stable metabolites TXB2,6 ─ Keto ─ PGF1α levels were measured. Results: (1) MDA content in asthma attack group (8.16 ± 1.58nmol / ml) was significantly higher than that in control group (6.08 ± 1.39nmol / ml) (p <0.001) GSH-Px activity were significantly lower (p less than 0.005,0.001 and 0.05), indicating that lipid oxidation in patients with asthma increased antioxidant capacity is low, plays an important role in the pathogenesis. (2) There was a significant linear negative correlation between serum MDA level and SOD activity (r = -0.481, p <0.025) in the asthma attack group, suggesting that the low antioxidant capacity may be the reason for the increased lipid peroxidation . (3) TXB2 level, TAB2 / 6-Keto-PGF1α level and 6-Keto-PGF1α level decreased in asthma attack group compared with control group, the difference was significant, indicating that TXA2-PGI2 imbalance involved in the pathogenesis of asthma. (4) There was a linear positive correlation between serum MDA level and TXB2 level in asthma attack group (r = 0.637, P <0.0025), but negatively correlated with 6-Keto-PGF1α level