摘要
目的探讨bcl-2、bax基因在兔骨关节炎软骨细胞凋亡中的意义。方法新西兰白兔12只,随机分为模型组,按照石膏外固定兔后膝关节造模,以及空白对照组,6周后处死动物取得膝关节软骨。采用免疫组织化学和原位杂交检测bcl-2、bax mRNA及蛋白表达。结果模型组软骨细胞bcl-2、bax mRNA表达明显多于对照组(P＜0．05)。免疫组织化学模型组软骨细胞bcl-2、bax阳性表达灰度值明显降低,与对照组比较差异有统计学意义(P＜0．05)；阳性细胞比例明显提高,与对照组比较差异有统计学意义(P＜0．01)。模型组bcl-2/bax阳性细胞率比值比对照组低,差异有统计学意义(P＜0．05)。结论bcl-2和bax共同参与了兔骨关节炎模型软骨细胞凋亡的调节,结果导致软骨细胞凋亡加快。
Objective To research the significance of genes bel-2 and bax in chondrocyte apoptosis in experimental osteoarthritis in rabbits. Method Twelve New Zealand rabbits divided into two groups at random： model group and control group. Model group with hoteoarthritis was duplicated by immobilizing with gypsum at extension position in right hind limb of rabbits. Rabbits of model group were executed after 6 weeks and chondrocytes were taken. Positive expression rate of bcl-2 and bax mRNA was measured by immunohistochemistry and Terminal deoxynucleotidyl transferase mediated dUTP nick end labeling （TUNEL）. Results Positive expression rate of mRNA in bcl-2 and bax of model group was obviously more than control group （P〈 0.05）. According to immunohistochemistry, and grey grade of positive expression of protein in bcl-2 and bax of chondrocytes in model group was lower and positive expression rate was gigher, compared with control group （P〈0.05, P〈0.01）. bcl-2 and bax of model group were lower than control group （P〈0.05）. Conclusion Genes bcl-2 and bax participate and thus accelerate chondrocyte apoptosis of osteoarthritis together.
出处
《中华风湿病学杂志》
CAS
CSCD
2006年第7期413-415,i0003,共4页
Chinese Journal of Rheumatology
基金
中国石化集团胜利石油管理局重点科研攻关资助项目(GKY0504)
