Ⅱ型胶原与Bcl-2在骨关节炎软骨细胞中的表达

Expression of type-Ⅱ collagen and Bcl-2 in articular chondrocyte of osteoarthritis

[目的]比较骨关节炎患者软骨细胞与正常软骨细胞内Ⅱ型胶原mRNA与Bcl-2mRNA的表达情况,分析两者间的关系,探讨两类骨关节炎发病机制的异同。[方法]收集原发性骨关节炎、继发性骨关节炎的关节软骨各8例,并以9例正常关节软骨作对照,采用逆转录/聚合酶链反应(reverse transcriptase/polymerase chain reaction,RT-PCR)方法检测Ⅱ型胶原mRNA与Bcl-2mRNA在骨关节炎软骨细胞和正常软骨细胞中的表达情况。[结果]原发性骨关节炎与继发性骨关节炎组Ⅱ型胶原mRNA的表达均明显低于正常组,差异均有统计学意义(P<0.01,P=0.014),而两类骨关节炎组间Ⅱ型胶原mRNA的表达差异没有统计学意义(P=0.716);Bcl-2 mRNA在原发性骨关节炎组与继发性骨关节炎组中的表达较对照组均升高(P<0.01,P<0.05),而两组间差异没有统计学意义(P>0.05)。[结论]软骨细胞内Ⅱ型胶原表达的减少直接导致了Ⅱ型胶原质和量的改变,是骨关节炎发病的重要环节,是两类骨关节炎发病的共同途径;Bcl-2是骨关节炎发病过程的重要调节因子,是软骨细胞和细胞外基质沟通的桥梁。

[ Objective] To explore the expression of type - Ⅱ collagen and Bcl -2 in osteoarthritis （OA） and normal hu- man articular chondrocyte. To investigate the differences of two type OA in pathomechanism. [ Methods] The samples of articu- lar cartilage were obtained from the patients undergoing total joint replacement, including 8 primary OA patients, 8 secondary OA patients and 9 normal subjects. Type - Ⅱ collagen and Bcl - 2 expression of chondrocyte were detected by reverse tran- scriptase/polymerase chain reaction （RT- PCR） . [Results] The expressin of type- Ⅱ collagen mRNA in normal OA group was higher than those in primary OA group and secondary OA group, there was significant difference between OA group and the normal control group （P 〈 0. 01, P = 0. 014 ） , while there was no significant difference between primary OA group and secondary OA group （P =0. 716） . The expressin of Bcl -2 mRNA in normal OA group was lower than those in primary OA group and secondary OA group, there was significant difference between OA group and the normal control group （ P 〈 0.01, P 〈 0.05 ） , while there was no significant difference between primary OA group and secondary OA group （P 〉 0. 05 ） . [ Conclusion] The reduction of type - Ⅱ collagen expression led to the change of collagen directly, which plays an important role in OA as well as common pathway of primary OA and secondary OA. The change of bcl - 2 expression is the key factor in the pathomechanism of OA. Bcl -2 is a link between extracellular matrix and cartilage cells.