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目的:研究血红素氧合酶-Ⅰ(HO-Ⅰ)是否参与单磷酰酯A诱导的心脏延迟保护作用.方法:在体大鼠心脏缺血-再灌损伤模型,缺血前24小时应用单磷酰酯A(500μg/kg,ip)诱导心脏延迟保护,观察单磷酰酯A对心肌梗死面积、肌酸激酶(CK)活性以及血清一氧化氮(NO)浓度的影响,并检测心脏HO-ⅠmRNA和蛋白的表达.结果:单磷酰酯A明显缩小心梗面积,减少CK释放以及显著升高血清NO浓度(P<0.01).这些作用可被预先给予一氧化氮合酶抑制剂L-亚硝基精氨酸甲酯(L-NAME,10mg/kg,ip)和血红素氧合酶抑制剂锌原叶啉LX(ZnPP-9,45μmol/kg,ip)所取消(P<0.01);单磷酰酯A明显增加心脏HO-ⅠmRNA和蛋白的表达,这一作用不被L-NAME所影响(P>0.05).结论:HO-Ⅰ/NO途径介导单磷酰酯A诱导的延迟心脏保护.
Objective: To investigate whether heme oxygenase-Ⅰ (HO-Ⅰ) is involved in the delayed protection of heart induced by monophosphatidic acid ester A. Methods: The model of ischemia-reperfusion injury in rat heart was established 24 hours before ischemia Monophosphoryl ester A (500μg / kg, ip) induced delayed protection of the heart to observe the impact of monophosphoryl ester A on myocardial infarct size, creatine kinase (CK) activity and serum nitric oxide (NO) HO-ⅠmRNA and protein expression.Results: Monophosphoryl ester A significantly reduced myocardial infarct size, decreased CK release, and significantly increased serum NO concentration (P <0.01) .These effects can be pre-given nitric oxide synthase inhibitor (L-NAME, 10 mg / kg, ip) and heme oxygenase inhibitor zinc protoporphyrin LX (ZnPP-9, 45 μmol / kg, ip) 0.01). Monophosphoryl ester A significantly increased the expression of HO-I mRNA and protein in heart, which was not affected by L-NAME (P> 0.05) .Conclusion: HO-Ⅰ / NO pathway mediates monophosphoryl ester A Induction of delayed cardioprotection.