摘要
目的通过检测动脉粥样硬化(AS)患者血液中基质金属蛋白酶-9(MMP-9)与基质金属蛋白酶抑制物-1(TIMP-1)的基因表达水平,探讨AS发生的分子机制及预测因子。方法 AS患者120例为动脉硬化组,72例正常体检者为对照组。用实时荧光定量PCR(RT-PCR)检测其血液中MMP-9和TIMP-1 mRNA表达水平。结果 MMP-9和TIMP-1的RT-PCR产物序列与GenBank上人MMP-9 mRNA和TIMP-1基因片段完全一致。动脉硬化组的MMP-9基因表达水平高于对照组MMP-9基因表达水平,但差异无统计学意义(P>0.05)。动脉硬化组的TIMP-1基因表达水平低于对照组TIMP-1基因表达水平,差异有统计学意义(P<0.05)。MMP-9/TIMP-1基因表达定量比值,动脉硬化组高于对照组,差异有统计学意义(P<0.05)。结论 AS患者TIMP-1基因表达水平的降低与MMP-9/TIMP-1基因表达定量比值升高可能是AS发生的分子机制之一,二者一起可以作为AS发生的预测因子。
Objective To observe matrix metalloproteinase-9(MMP-9) and matrix metalloproteinase inhibitor-1(TIMP-1) gene expression in the blood of the patients with atherosclerosis(AS).Methods One hundred and twenty patients with AS hospitalized and matched with diagnostic criteria were enrolled into experimental group.Seventy two cases who had accepted normal physical examination were enrolled into as the control group.The level of expression of MMP-9 and TIMP-1 mRNA in both the groups were detected by real-time fluorescence quantitative PCR(RT-PCR) technology.Results The sequence of RT-PCR products of MMP-9 and TIMP-1 was consistent with their human genetic fragment in GenBank. The level of expression of MMP-9 mRNA in the experimental group was higher than that in the control group,but there was not significant difference between two groups(P〉0.05 ).The level of expression of TIMP-1 mRNA in the experimental group was significantly lower than that in the control group,and there was significant difference(P〈0.05).The ratio of expression of MMP-9 and TIMP-1 mRNA was higher in experimental group than that in the control group,there was significant difference(P〈0.05).Conclusion The level of TIMP-1 gene expression decresed and the ratio of MMP-9/TIMP-1 mRNA expression increased in patients with AS can be one of the molecular mechanisms of the triggering and promotion factors in the prosedure of AS.Both of them can be taken as independent predictors of As in patients.
出处
《苏州大学学报(医学版)》
CAS
北大核心
2011年第1期118-120,123,共4页
Suzhou University Journal of Medical Science
基金
江苏省自然科学基金资助项目(BK2008117)