摘要
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。
AIM: The effect of cobra venom factor (CVF) on the number and action of leukocytes in rats with pulmonary injury induced by oleic acid was investigated. METHODS: Oleic acid (0. 1 mL' kg-1 iv ) was given to rats to induce pulmonary injuries which served as a pathological model of respiratory distress syndrome . CVF 1. 0 mg' kg-1ip, given to rats 24 h prior to oleic acid injection to deplete blood complement. The method of nitrite reaction was used for the superoxide dismutase (SOD)activity determination of leukocytes; and the method of phagocytose staphylococcus aureus for the phagocytic fonction;the blood cell counting plate for the adhesion function of leukocytes. RESULTS:CVF showed prominent effects against the action and SOD activity changes of leukocytes induced by oleic acid: decrease in leukocyte bacteriophagic percentage (from 52% ± 6%to 30% ± 5 % ), the leukocyte adherence percentage (from 93% ±11% to 82%±10% ); attenuate in production of oxygen free radicals, fall of SOD activity was significant prevented. However, there were no significan effect on the leukocytosis induced by oleic acid. CONCLUSION: Complement may be involved in the mediation of leukocyte action, and the protection mechanism that CVF could attenuate the pulmonary injuries may be related to the depression of leukocyte function caused by the complement depletion.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1999年第9期835-837,共3页
Chinese Journal of Pathophysiology
基金
国务院侨办重点学科科研基金!93-95-7
广东省自然科学基金!.974026