Matsuoka Y, Kitamura Y, Okazaki M, Terai K, Taniguchi T
Department of Neurobiology, Kyoto Pharmaceutical University, Yamashina, Japan.
Exp Brain Res. 1999 Jan;124(2):215-22. doi: 10.1007/s002210050616.
Nuclear factor-kappaB (NF-kappaB) is known to play a key role in immune and inflammatory responses. To understand the mechanisms of inflammatory activation that accompany neuronal damage, we determined the cell type in which NF-kappaB was activated. NF-kappaB protein was detected in the cytosolic fraction of untreated and vehicle-treated rat hippocampus. After kainic acid (KA) treatment, NF-kappaB protein was significantly increased in both the cytosolic and particulate fractions. NF-kappaB immunoreactivity was observed in both brain blood vessels and glial cells after 1 day. Although NF-kappaB immunoreactivity in brain blood vessels disappeared after 3 days, this activity was maintained in glial cells for up to 7 days. In addition, double immunostaining indicates that NF-kappaB was activated in glial cells, such as microglia and astrocytes, after 3 days. Thus, NF-kappaB activation seems to be delayed and to occur continuously in microglia and astrocytes, suggesting that an inflammatory activation in glial cells participates in KA-induced neurodegeneration.
已知核因子-κB（NF-κB）在免疫和炎症反应中起关键作用。为了解伴随神经元损伤的炎症激活机制，我们确定了NF-κB被激活的细胞类型。在未处理和用赋形剂处理的大鼠海马体的胞质部分中检测到NF-κB蛋白。在用海藻酸（KA）处理后，胞质和颗粒部分中的NF-κB蛋白均显著增加。1天后在脑血管和胶质细胞中均观察到NF-κB免疫反应性。尽管脑血管中的NF-κB免疫反应性在3天后消失，但这种活性在胶质细胞中维持长达7天。此外，双重免疫染色表明，3天后NF-κB在小胶质细胞和星形胶质细胞等胶质细胞中被激活。因此，NF-κB激活似乎延迟并在小胶质细胞和星形胶质细胞中持续发生，这表明胶质细胞中的炎症激活参与了KA诱导的神经退行性变。
