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为探讨单磷酰脂Ａ（ＭＬＡ）的心脏保护作用与诱导金属硫蛋白（ＭＴ）产生之间的关系，本实验在大鼠离体灌注心脏缺血再灌注（Ｉ／Ｒ）模型上观察ＭＬＡ预处理２４ｈ后，对心脏缺血再灌注损伤及ＭＴ含量的影响。结果发现，ＭＬＡ预处理增加心肌ＭＴ含量达４．６倍（ｐ＜０．０１），并增加了对Ｉ／Ｒ的抵抗，表现为改善了心功能和增加了心肌能量储备（ＡＴＰ含量升高）及抑制心肌酶和肌红蛋白的漏出。应用ＭＴ抗血清消除了ＭＬＡ预处理的心脏保护作用。结果表明，诱导ＭＴ产生可能是ＭＬＡ预处理心肌保护作用机理之一。
In order to explore the relationship between the cardioprotection of monophosphoryl lipid A (MLA) and the induction of metallothionein (MT), we observed the effects of MLA on I / R model Effects of 24 h preconditioning on cardiac ischemia / reperfusion injury and MT content. The results showed that MLA pretreatment increased myocardial MT content by 4.6-fold (p <0.01) and increased resistance to I / R as evidenced by improved cardiac function and increased myocardial energy reserve (increased ATP content ) And inhibition of myocardial enzymes and myoglobin leakage. The application of MT antiserum abolished the cardioprotective effect of MLA preconditioning. The results showed that the induction of MT production may be MLA pretreatment myocardial protection one of the mechanisms.