Matsuoka Y, Kitamura Y, Okazaki M, Sakata M, Tsukahara T, Taniguchi T
Department of Neurobiology, Kyoto Pharmaceutical University, Yamashina, Japan.
J Cereb Blood Flow Metab. 1998 Aug;18(8):824-32. doi: 10.1097/00004647-199808000-00002.
Recent studies strongly suggest that oxidative stresses participate in ischemia/reperfusion-induced neurodegeneration. In addition, heme oxygenase (HO) and major histocompatibility complex (MHC) antigens serve as functional molecules against oxidative stress and as self-recognition markers in the immune system, respectively. In this study, we examined the induction of HO and MHC antigens in the rat hippocampus after transient forebrain ischemia. The protein level of HO-1 was significantly enhanced after an episode of ischemia. After ischemia, HO-1 expression was observed early but transiently in the CA1 pyramidal neurons and later but continuously in glial cells. Glial cells expressing HO-1 were predominantly ameboid microglia, but not astrocytes. Ameboid microglia expressing HO-1 were predominantly localized with MHC class II antigens. These results indicate that (1) HO-1 expression in CA1 pyramidal neurons may be harmful, and (2) ischemia induces HO-1 in ameboid microglia that express MHC class II antigens, indicating a very specific microglial stress protein response.
最近的研究有力地表明，氧化应激参与了缺血/再灌注诱导的神经退行性变。此外，血红素加氧酶（HO）和主要组织相容性复合体（MHC）抗原分别作为对抗氧化应激的功能分子和免疫系统中的自我识别标志物。在本研究中，我们检测了短暂性前脑缺血后大鼠海马中HO和MHC抗原的诱导情况。缺血发作后，HO-1的蛋白水平显著升高。缺血后，HO-1在CA1锥体神经元中早期但短暂地表达，随后在胶质细胞中持续表达。表达HO-1的胶质细胞主要是阿米巴样小胶质细胞，而非星形胶质细胞。表达HO-1的阿米巴样小胶质细胞主要与MHC II类抗原共定位。这些结果表明：（1）CA1锥体神经元中HO-1的表达可能是有害的；（2）缺血诱导表达MHC II类抗原的阿米巴样小胶质细胞中HO-1的表达，表明存在一种非常特异的小胶质细胞应激蛋白反应。
