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退变腰椎间盘组织中细胞凋亡及相关基因bcl-2和bax表达的研究 被引量:7

Apoptosis of Disc Cells and Apoptotic Related Genes Bcl-2 and Bax in Degenerative Lumbar Disc Tissue
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摘要 目的:探讨腰椎间盘退变的发病机制。方法:采用原位DNA片段末端标记和免疫组织化学方法,检测40例退变腰椎间盘组织及10例正常腰椎间盘组织细胞凋亡状态及凋亡相关基因bcl-2和bax蛋白的表达。结果:40例退变腰椎间盘组织凋亡指数(AI)均值为70.51,bcl-2蛋白阳性细胞百分比为10.12%,bax蛋白阳性细胞百分比为54.56%。10例正常腰椎间盘组织AI均值为20.02,bcl-2蛋白阳性细胞百分比为53.46%,bax蛋白细胞百分比为10.54%。两组间AI均值、bcl-2蛋白表达、bax蛋白表达差异均有显著性意义(P均<0.05)。bcl-2蛋白表达越弱,bax蛋白表达越强,凋亡细胞数越多。结论:bcl-2和bax蛋白均参与了腰椎间盘组织中细胞凋亡的调节,并在腰椎间盘退行性变发生和发展中发挥着重要作用。 Objective: Our aim was to explore the degenerative mechanism of lumbar intervertebral disc-Methods : We detected the apoptotic status and the expression of bcl-2 and bax in 40 cases of degenerative lumbar intervertebral disc and 10 of normal lumbar inten'ertebral disc with TdT-mediated dUTP - biotin nick end labeling and immunohis-tochemistry methods. Results: The average apoptotic index (A1) in 40 cases of degenerative lumbar intervertebral disc was 70. 51 .significantly higher than that of 10 normal cases(20. 02) (P < 0.05). The expressions of bcl-2 and bax protein were in the chondrocytes of lumbar intervertebral disc tissues. The expression rate of bax protein in 40 cases of degenerative lumbar intervertebal disc was 54.56, significantly higher than that of 10 normal cases (10.54) (P < 0. 05). The expression rate of bcl-2 protein in 40 cases of degenerative lumbar intervertebral disc was 10. 12,significantly lower than that of 10 normal cases (53.46) (P < 0. 05). The higher bax and (or) the lower bcl-2 protein expressed,the bigger the apoptotic index was (P < 0. 01). Conclusion:Both bcl-2 and bax take part in the occurrence and progression of lumbar intervertebral disc degeneration .
出处 《中国医科大学学报》 CAS CSCD 北大核心 2003年第2期146-147,150,共3页 Journal of China Medical University
关键词 基因蛋白质 基因表达 腰推间盘退变 发病机制 免疫组织化学 intervertebral disc degeneration proteins gene expression
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