论文部分内容阅读
目的：观察眼镜蛇毒因子（CVF）对油酸型肺损伤大鼠外周血白细胞数目和功能的影响。方法：实验前24hCVF1mg·kg-1ip使补体耗竭。油酸0．1mL·kg-1iv致大鼠油酸型肺损伤病理模型。采用亚硝酸法测定白细胞SOD活力；白细胞吞噬功能测定则采用吞噬金葡菌法，粘附功能测定则采用玻璃血球计数板法。结果：CVF耗竭体内补体，能显著对抗油酸引起的白细胞吞噬和粘附功能的升高及超氧化物歧化酶（2）活性降低，使白细胞的吞噬率从（52±6）％下降至（30±5）％，粘附率从（93±11）％下降至（82±10）％；减少氧自由基的产生，白细胞SOD活性下降明显受到抑制。但对油酸引起的白细胞数目增加无明显影响。结论：CVF减轻油酸型肺损伤的作用机制可能与补体耗竭后引起的白细胞功能抑制有关。
Objective: To observe the effects of cobra venom factor (CVF) on the number and function of peripheral leukocytes in rats with oleic acid-induced lung injury. Methods: 24 hours before the experiment CVF1mg · kg-1ip complement depletion. The rat model of oleic acid induced lung injury induced by oleic acid 0.1 mL · kg-1iv. The nitrite method was used to determine the activity of leukocyte SOD; the phagocytosis of leucocytes was determined by the method of phagocytosis of Staphylococcus aureus; the adhesion function was determined by the glass plate counting method. Results: CVF exhausted body complement, which could significantly antagonize the increase of phagocytosis and adhesion of leucocytes and the decrease of superoxide dismutase (2) activity induced by oleic acid, and decreased the leukocyte phagocytosis rate from (52 ± 6)% to 30 ± 5)%. The adhesion rate decreased from (93 ± 11)% to (82 ± 10)%. Reducing the production of oxygen free radicals, the decrease of SOD activity in leukocytes was obviously inhibited. However, the number of white blood cells caused by oleic acid had no significant effect. CONCLUSION: The mechanism of CVF in reducing oleic acid-induced lung injury may be related to the inhibition of leukocyte function after complement depletion.