流感病毒相关脑病患者血清中MMPs和TIMP-1水平

Serum levels of MMPs and TIMP-1 in patients with influenza-virus-associated encephalopathy

目的: 观察基质金属蛋白酶(MMPs)及金属蛋白酶组织抑制剂(TIMPs)在流感病毒相关脑病 (简称流感脑病)发病机制中的作用。方法:应用ELISA检测 22例流感脑病患儿, 20例同年龄的流感病毒感染但无脑病患儿及 22例同年龄的非感染性神经疾病患儿血清MMP-2,MMP -9和TIMP 1。结果:脑病组及流感组血清MMP -9水平均高于对照组,但脑病组与流感组之间无明显差别;流感组及脑病组的MMP -2水平均较对照组明显减低,而且脑病组也较流感组明显减低;TIMP- 1在脑病组中的水平较对照组明显升高,但与流感组比较无明显升高;可反映蛋白分解能力的MMP- 9 /TIMP- 1比率在脑病和流感组中均明显升高。结论:流感脑病病人血清MMP- 9增高,MMP- 2下降,表明MMPs可能参与了流感脑病的发病。

Objective: To evaluate the role of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinase-1(TIMP-1)in the pathogenesis of influenza-virus-associated encephalopathy (Flu encephalopathy). Methods:We measured MMP-2, MMP-9, and TIMP-1 levels in serum samples of 22 patients with Flu encephalopathy by using the enzyme-linked-immunosorbent assay (ELISA). The results were compared with those of 20 age-matched patients with influenza virus infection without encephalopathy and 22 age-matched patients with noninfectious neurologic diseases. Results:The levels of MMP-9 were eminently elevated in patients with influenza and Flu encephalopathy compared with the control group. Howerer, no difference was found in MMP-9 between patients with influenza and Flu encephalopathy. The MMP-2 was eminently decreased in patients with influenza and Flu encephalopathy compared with the control group (P<0.05). There was significant difference in MMP-2 level between patients with influenza and Flu encephalopathy. Although the level of TIMP-1 in patients with Flu encephalopathy was significantly higher than that in control group, the TIMP-1 was not significantly up-regulated in patients with Flu encephalopathy compared with influenza group (P>0.05). The ratio of MMP-9 to TIMP-1 ratio, a measure of proteolytic capacity, was strongly increased in patients with Flu encephalopathy and influenza. Conclusion:The investigations of serum samples of patients with Flu encepholopathy revealed the increase of MMP-9 and decrease of MMP-2, suggesting that MMPs may be involved in the pathophysiology of Flu encepholopathy in humans.