MMP-9及PPARγ与2型糖尿病动脉粥样硬化

Matrix metalloproteinase-9,PPARγ and atherosclerosis of type 2 diabetes

基质金属蛋白酶-9(MMP-9)是一种降解细胞外基质的蛋白酶,能促进动脉粥样硬化(AS)斑块的形成、发展及破裂,在AS病变时明显增高。已发现高糖可诱导其表达,在2型糖尿病合并AS中更是显著升高。抑制其生成,改善细胞外基质重构已成为2型糖尿病治疗的方向之一。过氧化物酶体增殖物活化受体(PPAR)γ是核受体超家族成员,可调控靶基因转录,从多方面发挥抗AS的作用,其中一个关键环节就是抑制MMP-9的表达。PPARγ激动剂(噻唑烷二酮类降糖药)应用于2型糖尿病合并AS,不仅有效降糖、降脂,改善胰岛素抵抗,而且抑制MMP-9表达,抑制AS的形成和进展。

Matrix metalloproteinase-9（MMP-9）is a kind of enzyme which can contribute to the atherosclerotic plaque formation, progression and rupture by degrading extracellular matrix, It is increased in the patients with atherosclerosis. Hyperglycemia can induce its expression and it is increased significantly in the type 2 diabetic patients with atherosclerosis. So reducing its levels, improving the remodeling of extracellular matrix have become the important therapeutic measurement in type 2 diabeles. Proxisome proliferator-activated receptor-gamma（PPART） is the member of nuclear receptor superfamily. It modulates the transcription of target genes, has antiatherosclerotic effects in many aspects. A key aspect is to inhibit the expression of MMP-9, PPARγ agonist（thiazolidinedione） can not only reduce blood glucose, blood lipids, improve insulin resistance, but also inhibit the production of MMP-9 and the formation and progression of atherosclerosis in type 2 diabetic patients.