赖诺普利对仓鼠心肌梗死后基质金属蛋白酶-9活性的抑制作用
Inhibition of matrix metalloproteinase-9 activity by lisinopril after myocardial infarction in hamsters.
作者信息
Takai Shinji, Yamamoto Daisuke, Jin Denan, Inagaki Sachiko, Yoshikawa Katsuhiro, Tanaka Kazuhiko, Miyazaki Mizuo
机构信息
Department of Pharmacology, Osaka Medical College, Takatsuki City, Osaka 589-8686, Japan.
出版信息
Eur J Pharmacol. 2007 Jul 30;568(1-3):231-3. doi: 10.1016/j.ejphar.2007.04.036. Epub 2007 Apr 30.
We measured angiotensin-converting enzyme and matrix metalloproteinase-9 activities after myocardial infarction in hamsters and compared the effects of an angiotensin-converting enzyme inhibitor lisinopril with those of an angiotensin receptor blocker candesartan cilexetil after myocardial infarction. Angiotensin-converting enzyme activity was significantly increased 3 and 7 days, but not 1 day after myocardial infarction. Matrix metalloproteinase-9 activity was significantly increased 1 day after myocardial infarction. Lisinopril significantly inhibited both angiotensin-converting enzyme and matrix metalloproteinase-9 activities, but candesartan cilexetil did not. Angiotensin-converting enzyme inhibitors might directly inhibit matrix metalloproteinase-9 activity.
我们测定了仓鼠心肌梗死后血管紧张素转换酶和基质金属蛋白酶-9的活性，并比较了血管紧张素转换酶抑制剂赖诺普利与血管紧张素受体阻滞剂坎地沙坦酯在心肌梗死后的作用。心肌梗死后1天，血管紧张素转换酶活性未显著增加，但在3天和7天时显著升高。心肌梗死后1天，基质金属蛋白酶-9活性显著增加。赖诺普利显著抑制血管紧张素转换酶和基质金属蛋白酶-9的活性，但坎地沙坦酯没有。血管紧张素转换酶抑制剂可能直接抑制基质金属蛋白酶-9的活性。
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