骨碎补对膝骨性关节炎模型兔滑膜细胞凋亡机制的实验研究

Rhizoma Drynariae on Synovial Cells Apoptosis of Rabbits with Osteoarthritis

目的:观察骨碎补对兔膝骨性关节炎滑膜细胞凋亡Fas、Fasl蛋白因子的影响。方法:将24只新西兰兔随机分为正常组、模型组、骨碎补治疗组、维固力(硫酸氨基葡萄糖)对照组,每组6只实验动物。采用左后肢伸直位管型石膏固定的方法造成膝骨性关节炎的动物模型,固定时间为6周。造模成功后,治疗组按1.5 g/(kg·d)剂量灌胃给予骨碎补,对照组按70 mg/(kg·d)剂量灌胃给予硫酸氨基葡萄糖,模型组和正常组按同等剂量胃饲给予生理盐水。治疗4周后,观察滑膜细胞形态学改变、滑膜细胞凋亡情况及Fas、Fasl蛋白表达水平。结果:骨碎补治疗组、硫酸氨基葡萄糖对照组TUNEL阳性标记的滑膜细胞数均较多,高于正常组(P<0.01),却显著低于模型组,差异有统计学意义(P<0.01)骨碎补治疗组、硫酸氨基葡萄糖对照组均可以下调兔膝OA模型Fas、Fas L的表达,其蛋白表达水平明显高于正常组(P<0.01),低于模型组(P<0.01)。两组组间比较,差异有显著性,说明骨碎补下调Fas、Fas L的蛋白表达水平强于硫酸氨基葡萄糖。结论:骨碎补能抑制骨性关节炎滑膜细胞的过度凋亡且效用优于硫酸氨基葡萄糖。

Objective： To explore the influence of Rhizoma Drynariae on Fas and Fasl in synovial cell apoptosis of knee osteoarthritis rabbits. Method： Twenty- four New Zealand white rabbits were randomly divided into normal group,model group,treatment group and glucosamine sulfate group,each group 6 only. The left hind limb extension was used for establishing the animal model of knee osteoarthritis,fixing for 6 weeks. After the success of modeling,the treatment group was given Rhizoma Drynariae according to 1. 5 g /（ kg·d） dosage by intragastric administration and the control group given glucosamine sulfate according to 70 mg /（ kg · d） dosage by intragastric administration. The model and normal groups were given normal saline by gastric feeding the same dose. After 4 weeks of treatment,observe Fas and Fasl protein expression levels by Western- Blot method. Results： Rhizoma Drynariae treatment and control groups＇ number of synovial cells with TUNEL positive markers were more,higher than the normal group＇s（ P〈0. 01） and significantly lower than that in the model group. The differences were statistically significant（ P〈0. 01）. Rhizoma Drynariae and glucosamine sulfate can reduce Fas and Fas L expressions which were higher than the normal group＇s（ P〈0. 01） and lower than that of model group（ P〈0. 01）. Comparison between the two groups had a significant difference between the expressions of Fas and Fas L. Conclusion： Rhizoma Drynariae can inhibit synovial cells excessive apoptosis in osteoarthritis and is better than the glucosamine sulfate.