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作者研究了45例哮喘发作者和34例健康对照者血淋巴细胞化学发光强度(Ly-cl),多形核白细胞化学发光强度(PMN-cl),超氧化物歧化酶(SOD),谷胱甘肽过氧化物酶(GSH-Px)活性和血浆丙二醛(MDA)含量的变化。结果显示,哮喘发作组Ly-cl和PMN—cl较对照组显著增强(P<0.05),说明在哮喘发作组Ly和PMN的自由基代谢功能增强。全血GSH-Px活力较对照组明显下降(P<0.05),而血浆SOD活力显著增高(P<0.05),血浆MDA含量明显增多(P<0.05)。表明,体内Ly及PMN活化而释放的过多活性氧(OR)以及由于抗氧化功能的受损而产生的脂质过氧化可能是哮喘发病的机制之一。
The authors studied the changes of Ly-cl, PMN-cl, SOD, and glutathione peroxidase in 45 asthmatic patients and 34 healthy controls. Changes of GSH-Px activity and plasma malondialdehyde (MDA) levels were observed. The results showed that Ly-cl and PMN-cl in the asthma attack group were significantly higher than those in the control group (P <0.05), indicating that the free radical metabolism of Ly and PMN in the asthma attack group was enhanced. The activity of GSH-Px in whole blood was significantly lower than that of the control group (P <0.05), while the activity of SOD in plasma increased significantly (P <0.05) and the content of MDA in plasma increased significantly (P <0.05). It is suggested that excess reactive oxygen species (ROS) released by activation of Ly and PMN in vivo and lipid peroxidation due to the impairment of antioxidant function may be one of the mechanisms of asthma pathogenesis.