摘要
目的 :探讨氧自由基对大面积严重烧伤后红细胞膜补体受体 1型分子 (CR1)数量表达水平变化 (即活性变化 )的影响。方法 :于伤后 1天、 3天、 5天、 7天、 14天、 2 1天、 2 8天、 35天 ,采用酶联免疫 (ELISA)法测定红细胞CR1分子数量 ,同时采用化学比色法检测血浆丙二醛 (MDA)、超氧化物歧化酶 (SOD)和谷胱甘肽过氧化物酶 (GSH PX ) ,观察其水平的变化 ,并进行相关性分析。结果 :①患者伤后红细胞CR1分子表达水平显著低于对照组 (P <0 0 1)但伤后 2 8天后逐渐恢复至正常 ;②伤后SOD和GSH PX的水平显著下降 ,MDA的水平显著上升 ,至少伤后 2 1天才逐渐恢复至正常水平 ;③红细胞CR1分子表达水平与SOD和GSH PX的水平呈高度正相关 (r=0 90 4、P <0 0 1;r=0 938、P<0 0 0 1) ;与MDA的水平呈高度负相关 (r=0 86 0、P <0 0 1)。结论 :红细胞膜极易产生脂质过氧化作用 ,烧伤后自由基损伤的程度可直接影响红细胞膜的功能 ,特别是红细胞膜CR1分子表达降低和红细胞免疫粘附功能 (RCIA)降低 ,提示减少机体自由基的产生 。
Objective: To investigate the effect of oxygen free radical on the expression of erythrocyte CR1 molecule post large area severe burn. Method: Patients with large area and sever burn had their blood sample collected on day 1,3,5,7, 14, 21, 28 and 35 post burn. The amount of erythrocyte CR1 molecule was measured using ELISA method, and plasma MDA, SOD and GSH-PX levels were measured using colorimetric method. Correlation analysis of the changes in the levels was made. Result: 1. Patients had erythrocyte CR1 molecule expression level significantly lowered post burn, compared with the normal control (P<0.01), and was gradually recovered after 28 days post burn. 2. SOD and GSH-PX levels were significantly lowered post burn, and began to recover at least after 21 days post burn. 3. Erythrocyte CR1 molecule expression level was positively correlated to SOD and GSH-PX levels (r=0.904, P<0.01; r=0.938, P<0.01), while it was negatively correlated to MDA level (r=-0.860, P<0.01). Conclusion: Lipid peroxidation often takes place at the erythrocyte membrane post burn. Free radical injury may directly influence the function of the erythrocyte membrane, as a result, erythrocyte CR1 molecule expression level and RCIA function were lowered. This result suggests that it is very important to reduce the production of free radicals and to promote RCIA function of burn patients.
出处
《中国烧伤创疡杂志》
2004年第2期89-92,共4页
The Chinese Journal of Burns Wounds & Surface Ulcers
关键词
烧伤
补体受体
氧自由基
红细胞免疫
Burn
complement receptor
oxygen free radical
red corpuscle immunity
