金属硫蛋白在培养乳鼠心肌细胞缺氧预处理中的作用

Protective mechanism of metallothionein on cultivated rat cardiomyocytes in hypoxic preconditioning

目的：探讨金属硫蛋白（ＭＴ）在培养乳鼠心肌细胞缺氧预处理中的作用机制。方法：建立培养的乳鼠心肌细胞缺氧／复氧模型，检测心肌细胞预缺氧２４ｈ后ＭＴ及丙二醛（ＭＤＡ）含量，Ｎａ＋－Ｋ＋ＡＴＰ酶、Ｃａ２＋－Ｍｇ２＋ＡＴＰ酶活性的变化以及用ＭＴ抗体阻断后的相应变化。结果：缺氧预处理组ＭＴ含量及Ｎａ＋－Ｋ＋ＡＴＰ酶、Ｃａ２＋－Ｍｇ２＋ＡＴＰ酶活性显著高于对照组及缺氧／复氧组（Ｐ＜０．０５），ＭＤＡ含量显著低于缺氧／复氧组（Ｐ＜０．０１）；使用ＭＴ抗体后，酶活性则显著降低，而ＭＤＡ含量显著高于未加抗体和对照组（Ｐ＜０．０１）。结论：缺氧预处理产生大量 ＭＴ，后者可能通过减少 ＭＤＡ及促进 Ｎａ＋－ Ｋ＋ ＡＴＰ酶、Ｃａ２＋－ Ｍｇ２＋ ＡＴＰ酶的活性升高起到保护心肌的作用。

AIM: Studying the mechanism of protective role of metallothionein (MT) in hypoxic preconditioning(HPC) of cultivated rat cardiomyocytes. METHODS: Using the model of hypoxia/reoxygenation of cultivated rat cardiomyocytes. Determing the contents of MT, malonyldialdehyde (MDA) - metabolism product of lipid peroxidation and the activities of Na+ - K+ ATPase, Ca2+ - Mg2+ ATPase of cardiomyocytes 24 h after HPC, the determining the relevant changes after using MT antibody. RESULTS: After 24 h in HPC, the contents of MT and activities of Na+ - K+ ATPase, Ca2+ - Mg2+ ATPase were obviously higher than those in the control and hypoxia/reoxygenation(P＜ 0. 05 ), and the contents of MDA were decreased remarkedly (P ＜ 0.01 ). Then after using MT antibody, the activities of two enzyme were progressively decreased and the contents of MDA were significanily higher than those in the control and MT antibody - free groups(P ＜ 0.01 ). CONCLUSION: HPC may induce excessive synthesis of MT, and MT can protect myocardial reoxygenation injury by eliminating lipid peroxidation and rising the activities of Na+ - K+ ATPase and Ca2+ - Mg2+ ATPase.