The mechanism of sinusoidal endothelial cell apoptosis induced by hydrogen peroxide derived from hepatocytes in hypoxic liver

Bcl-2现在被认为是凋亡细胞死亡的有效抑制剂。在这项研究中，我们探讨了肝窦内皮细胞凋亡诱导氢和肝保护Bcl-2的机制。在这里，我们报告说，缺氧诱导黄嘌呤氧化酶依赖的过氧化氢在肝细胞的生产，这扩散到窦内皮细胞和诱导选择性窦内皮细胞凋亡的血液灌注大鼠肝脏。另一方面，我们报道Bcl-2定位于线粒体、内质网和核膜，并且Bcl-2在正常大鼠肝脏中表达，主要定位于线粒体的内膜和嵴，而不是外膜。

Bcl-2 is now recognized as a potent inhibitor of apoptotic cell death. In this study, we investigated the mechanism of sinusoidal endothelial cell apoptosis induced by hydrogen and liver protection using Bcl-2. Here we report that hypoxia induces xanthine oxidase-dependent hydrogen peroxide production in hepatocytes, and that this diffuses into sinusoidal endothelial cells and induces selective sinusoidal endothelial cells apoptosis in the blood-perfused rat liver. On the other hand, we reported that Bcl-2 is located in the mitochondria, endoplasmic reticulum, and nuclear membrane and that Bcl-2 is expressed in normal rat liver, and locatedpredominantly in the inner membrane and crista rather than in the outer membrane of mitochondria.