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一氧化氮 (NO)在骨关节炎和关节软骨代谢中具有重要的病理生理作用。为研究NO与关节软骨II型胶原的关系 ,我们在培养的兔关节软骨细胞中以药物刺激产生NO后 ,分别用ELISA及RT -PCR法测定II型胶原及前II型胶原α1链 (COL2A1)mRNA表达量的变化。结果表明 ,0 2mM的硝普钠 (SNP)可释放出大量NO ,使软骨细胞II型胶原的含量减低 ,同时 ,RT -PCR法证实前II型胶原mRNA表达量也减少。 10 0u/ml白细胞介素 - 1(IL - 1)可刺激软骨细胞释放NO并使II型胶原量降低 ,其COL2A1mRNA表达量也减少。加用 1mg/ml精氨酸甲酯 (NAME ,NO合酶抑制剂 )后 ,则抑制了IL - 1的作用 ,使NO产量下降 ,II型胶原含量部分恢复 ,COL2A1完全恢复。本试验证实了NO作为IL - 1的下游分子抑制II型胶原的合成 ;其抑制作用是通过减少前II型胶原α1链mRNA表达量完成的。这在软骨细胞反分化过程中具有重要意义
Nitric oxide (NO) has an important pathophysiological role in osteoarthritis and articular cartilage metabolism. To study the relationship between NO and articular cartilage type II collagen, we produced type II collagen and pre-type II collagen alpha 1 chain (COL2A1) by ELISA and RT-PCR respectively after stimulated NO production in rabbit articular chondrocytes. Changes in mRNA expression. The results showed that 0 2mM sodium nitroprusside (SNP) could release a large amount of NO, which reduced the content of type II collagen in chondrocytes. Meanwhile, the expression of pre-type II collagen mRNA was also confirmed by RT-PCR. Interleukin - 1 (IL - 1) at 10 0u / ml stimulated the release of NO from chondrocytes and decreased the amount of type II collagen, as well as decreased the expression of COL2A1 mRNA. The addition of 1 mg / ml arginine methyl ester (NAME, NO synthase inhibitor) inhibited the effect of IL - 1, decreased NO production, partial recovery of type II collagen, and complete recovery of COL2A1. This experiment confirmed that NO acts as a downstream molecule of IL - 1 and inhibits the synthesis of type II collagen. Its inhibition is mediated through the reduction of mRNA expression of pre - type II collagen. This is of great importance in the process of chondrocyte dedifferentiation