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强力霉素通过调节局灶性脑缺血中的纤溶酶原激活剂来抑制基质金属蛋白酶。

Doxycycline inhibits MMPs via modulation of plasminogen activators in focal cerebral ischemia.

作者信息

Burggraf Dorothe, Trinkl Andreas, Dichgans Martin, Hamann Gerhard F

机构信息

Department of Neurology, Ludwig-Maximilians University, Klinikum Grosshadern, Marchioninistr. 15, 81377 Munich, Germany.

出版信息

Neurobiol Dis. 2007 Mar;25(3):506-13. doi: 10.1016/j.nbd.2006.10.013. Epub 2006 Dec 12.

Abstract

Tetracyclines inhibit matrix metalloproteinases (MMPs) and reduce infarction volume following cerebral ischemia. In this thesis an involvement of urokinase could be proven. Cerebral ischemia in rats was induced for 3 h followed by 24 h reperfusion (suture model). Each 6 animals received orally either doxycycline or water. Doxycycline treatment began 10 days before ischemia. MMP-2 and MMP-9 were substantially decreased. The possibility of involvement of the endogenous MMP inhibitors in the MMP inhibiting mechanisms was excluded. The plasminogen activator uPA was significantly decreased by doxycycline indicating an MMP inhibiting mechanism including the plasminogen/plasmin system. In the doxycycline group, this resulted in a decreased damage to the cerebral microvessels and less loss of the basal lamina antigen collagen type IV. Hemoglobin extravasation was also significantly reduced. Our results suggest that doxycycline may have a potential use as an anti-ischemic compound since it provides microvascular protection by inhibiting the plasminogen system.

摘要

四环素可抑制基质金属蛋白酶(MMPs),并减少脑缺血后的梗死体积。在本论文中,已证实尿激酶参与其中。对大鼠进行3小时的脑缺血诱导,随后进行24小时的再灌注(缝线模型)。每6只动物口服强力霉素或水。强力霉素治疗在缺血前10天开始。MMP-2和MMP-9显著降低。排除了内源性MMP抑制剂参与MMP抑制机制的可能性。强力霉素使纤溶酶原激活剂uPA显著降低,表明包括纤溶酶原/纤溶系统在内的MMP抑制机制。在强力霉素组中,这导致对脑微血管的损伤减少,基底膜抗原IV型胶原的损失减少。血红蛋白外渗也显著减少。我们的结果表明,强力霉素可能具有作为抗缺血化合物的潜在用途,因为它通过抑制纤溶酶原系统提供微血管保护。

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