BMP-7與IL-6對(duì)人髓核細(xì)胞ColⅡ與TIMP-1基因表達(dá)的影響

[摘要] 目的 探討不同濃度BMP-7與IL-6作用于體外培養(yǎng)的人髓核細(xì)胞對(duì)Ⅱ型膠原與TIMP-1基因表達(dá)的影響。方法 應(yīng)用逆轉(zhuǎn)錄聚合酶鏈反應(yīng)(RT-PCR)半定量檢測(cè)不同濃度BMP-7與IL-6作用下體外培養(yǎng)的人髓核細(xì)胞中TIMP-1和Ⅱ型膠原基因的表達(dá)量。結(jié)果 IL-6可以下調(diào)Ⅱ型膠原基因和 TIMP-1基因表達(dá);低濃度的BMP-7可以抵消相同濃度IL-6對(duì)髓核細(xì)胞的保護(hù)作用，高濃度的BMP-7可以促進(jìn)Ⅱ型膠原基因和TIMP-1基因表達(dá)。結(jié)論 BMP-7可以對(duì)抗IL-6作用和正向調(diào)節(jié)椎間盤細(xì)胞Ⅱ型膠原基因及TIMP-1基因表達(dá)，提示 BMP-7在臨床治療中可能具有逆轉(zhuǎn)早期椎間盤退變的作用。

[關(guān)鍵詞] IL-6;BMP-7;TIMP-1;Ⅱ型膠原;髓核細(xì)胞

[中圖分類號(hào)] R681.5+5 [文獻(xiàn)標(biāo)識(shí)碼] A [文章編號(hào)] 1673-9701(2010)04-24-03

Interaction of Bone Morphogenetic Protein-7 and Interleukin-6 on Gene Expression of TypeII-collagen and TIMP-1 in Human Nucleus Pulposus Cells in Vitro Cultured

FENG JunxiMA Xun*ZHANG LiWU XiaofeiHE Liming

Department of Orthopaedics，the Second Affiliated Hospital，Shanxi Medical University，Taiyuan 030001，China

[Abstract] Objective To discuss the interaction of different concentrations of bone morphogenetic protein-7(BMP-7) and interleukin-6(IL-6) on gene expression of typeⅡ-collagen and TIMP-1 in the in vitro cultured human nucleus pulposus cells. Methods We used the RT-PCR semi-quantitative detection of the gene expression levels of typeⅡ-collagen and TIMP-1 in the in vitro cultured human nucleus pulposus cells under the action of different concentrations of BMP-7 and IL-6. Results IL-6 reduced the gene expression levels of type II collagen and TIMP-1，and low concentration of BMP-7 could counteract the effects of the same concentration of IL-6 to protect the nucleus pulposus cells. High concentration of BMP-7 could promote the gene expression of typeⅡ-collagen and TIMP-1. Conclusion BMP-7 can antagonize the effects of IL-6 and regulate positively the gene expression of type II collagen an d TIMP-1 in the nucleus pulposus cells，suggesting BMP-7 could reverse the degeneration of intervertebral discs in the early stage of clinical treatment.

[Key words] Interleukin-6;Bone morphogenetic protein-7;Tissue inhibitors of matrix metalloproteinase-1;Type II-collagen;Nucleus pulposus cells

椎間盤退變(intervertebral disc degeneration，IDD)的病因十分復(fù)雜，其中細(xì)胞外基質(zhì)成分的合成減少和降解增加是造成椎間盤退變的重要因素之一。隨著對(duì)椎間盤退變基礎(chǔ)研究的逐步深入，細(xì)胞外基質(zhì)在椎間盤退變病理機(jī)制中的作用日益受到重視。關(guān)于TIMP-1及Ⅱ型膠原相關(guān)實(shí)驗(yàn)證實(shí)，退變髓核細(xì)胞中TIMP-1和Ⅱ型膠原基因表達(dá)明顯減少。椎間盤退變過(guò)程中有多種因子共同參與，IL-6是一種重要的炎性因子，能抑制成纖維細(xì)胞合成膠原，通過(guò)影響椎間盤髓核組織中的基質(zhì)降解酶的抑制酶而產(chǎn)生效應(yīng)的[1];而骨形態(tài)發(fā)生蛋白(BMP-7)具有促進(jìn)椎間盤細(xì)胞增殖及促進(jìn)細(xì)胞外基質(zhì)合成的能力[2]。本實(shí)驗(yàn)主要觀察椎間盤退變過(guò)程中的重要參與者IL-6與BMP-7對(duì)TIMP-1與Ⅱ型膠原基因表達(dá)的影響，進(jìn)一步探討IL-6 和BMP-7因子在椎間盤退變過(guò)程中的相互作用，為將來(lái)臨床有效的治療椎間盤退變提供理論和實(shí)驗(yàn)依據(jù)。……