大鼠背部气囊滑膜炎模型的探讨

Research of the inflammation model of the rats gasbag synovitis

目的:探讨不同致炎剂致大鼠背部气囊滑膜炎模型的特点。方法:实验第1d和第3d大鼠皮下注射空气20ml;第6d,大鼠皮下注射空气10ml,然后向气囊内注入不同致炎剂———角叉菜胶(Car)和脂多糖(LPS),观察不同浓度各致炎剂作用大鼠背部皮下气囊炎症发生、发展情况及对炎症因子的影响。结果:Car各剂量致炎组均可促进大鼠背部气囊滑膜炎炎性液的渗出,促进渗出液中白细胞聚集,升高渗出液总蛋白、NO、MDA和PGE2的含量,升高血清MDA含量和降低血清SOD活力,实验剂量Car100mg/kg、150mg/kg下,与空白对照组相比具有显著性差异。LPS致炎组在实验剂量下,对大鼠气囊滑膜炎炎性渗出液的渗出量、渗出液中MDA含量和血清SOD活力与空白对照组相比差异不显著,但对渗出液中总蛋白、NO、MDA和PGE2的含量的影响,随致炎剂量的增加,呈现出先升高后降低的趋势。结论:向大鼠皮下气囊注入角叉菜胶或脂多糖均可成功建立大鼠背部气囊滑膜炎模型。综合比较提示,Car(100mg/kg)大鼠背部气囊滑膜炎模型能较好地模拟在单一致炎因子存在情况下引起的炎症状态。

To explore the characteristics of different proinflammatory agent caused the rats gasbag synovitis model. Method： Experi- ments I d and 3d air to the subcutaneous injection of 20ml; the rats were injected air 10ml in 6d. The inflammation was induced by injecting two kinds of proinflammatory substances （ carrageenan or lipopolysaccharide） with different concentrations into subcutaneous air pouches of rats. The progress of inflammation and the influence on inflammatory factors were recorded. Results： Each dose proinflammatory Car group can promote inflammatory fluid oozing the dorsal air bag synovitis, promoting exudate leukocyte aggregation, increased exudate total protein content of NO, MDA and PGE2, elevated serum levels of MDA content and lower serum SOD activity experimental dose Car 100mg/kg, 150mg/kg, compared with the blank control group, with significant differences. LPS induced inflammation group in the experimental doses, rats airbags synovitis inflammatory exudate oozing exudate MDA content and serum SOD activity and the control group, the difference was not significant, but the exudatethe total protein content of NO, MDA and PGE2, with the cause of the increase in the dose of the inflammation, showing a trend first and then decreased. Conclusion： The rat subcutaneous air bag injection carrageenan or lipopolysaecharide rats airbags synovitis model can be successfully established. Comprehensive comparison prompted Car （100mg/kg） the rat air bag synovitis model can simulate in a single consistent inflammatory cytokines in the presence of inflammatory state caused.