山茱萸总苷对缺氧/复氧损伤乳鼠心肌细胞线粒体超微结构的影响

Effect of Total Glycosides from Shanzhuyu(Cornus officinalis) on Mitochondrion Ultrastructure of Myocardial Cells in Suckling Mouse with Hypoxia/Reoxygenation Injury

目的:观察山茱萸总苷对缺氧/复氧损伤乳鼠心肌细胞线粒体超微结构的影响,探讨其抗心肌细胞凋亡的作用机制。方法:将原代培养3 d的心肌细胞采用液体石蜡封闭法建立缺氧/复氧模型,分为正常组、缺氧/复氧模型组(缺氧2 h/复氧1 h)及药物干预组(缺氧/复氧前24 h及缺氧同时给予山茱萸总苷预处理),药物浓度分别为0.1、1.0、10 g/L.。电镜下观察各组心肌细胞线粒体的形态。结果:与正常对照组比较,模型组心肌细胞线粒体肿胀、膜破裂、嵴溶解融合或有电子致密颗粒沉积,给予山茱萸总苷干预后,中、高剂量组心肌细胞超微结构损伤程度明显改善,肌纤维排列基本整齐规则、线粒体完整、嵴清晰及未见空泡形成,低剂量组与模型组差异不明显。结论:山茱萸总苷可以抑制缺氧/复氧损伤对乳鼠心肌细胞超微结构的破坏,保护线粒体,可能是通过阻断心肌细胞凋亡线粒体通路去实现对心肌细胞的保护作用。

Objective： To observe the effects of total Glycosides from Cornus officinalis on ultrastructure of mitochondrion of cardiac muscle cells in suckling mouse with hypoxia / reoxygenation injury and explore the mechanism of its protection on apoptosis of cardiac muscle cells. Methods： The generation of 3 days training myocardial cells were divided to normal group,hypoxia / reoxygenation group（ hypoxia 2 h / reoxygenation 1 h） and drug group（ the drug was given 24 hours before hypoxia / reoxygenation and the same time）,drug concentration respectively was 0. 1 g / L,1 g / L and 10 g / L. Electron microscopy was used to observe the mitochondrion changes of myocardial cells. Results： Compared with normal group,hypoxia / reoxygenation group showed mitochondrial swelling,membrane rupture,cristae and electron dense granular deposition. With the intervention of total Glycosides from Cornus officinalis,the degree of damage in the ultrastructure of myocardial cells was improved obviously in middle and high dose group,the arrangement of muscle fiber was regular,the mitochondrion was completion and the cavitation could not be seen,but there was no significance difference between the low dose group and the model group. Conclusion： Total Glycosides from Cornus officinalis could inhibit the destruction to myocardial cells with hypoxia / reoxygenation injury,protect the mitochondrion,improve the ability of myocardial cells to hypoxia and ischemia. The mechanism of that may be by blocking the myocardial mitochondria apoptosis pathway to reach the protection of myocardial cells.