Popivanova Boryana K, Koike Koji, Tonchev Anton B, Ishida Yuko, Kondo Toshikazu, Ogawa Satoshi, Mukaida Naofumi, Inoue Masaki, Yamashima Tetsumori
Department of Obstetrics and Gynecology, Kanazawa University Graduate School of Medical Science, Takara-machi 13-1, Japan.
Brain Res. 2003 Apr 25;970(1-2):195-204. doi: 10.1016/s0006-8993(03)02343-6.
ELR(+) CXC chemokines including IL-8 are known to be involved in the ischemia-reperfusion injuries in various organs including rodent brain. However, the roles of these chemokines during the ischemia-reperfusion injuries of the primate brain still remain unknown. Here, we studied expressions of CXC chemokines and their receptor CXCR2 in monkey hippocampus known to develop total CA1 neuronal loss on day 5 after 20-min ischemia and reperfusion. ELR(+) chemokines and their receptor CXCR2 were not detected in the hippocampus of non-ischemic monkeys. On the contrary, at 30-60 min after the start of reperfusion, CD68-positive microglial cells increased significantly in the hippocampal CA1 sector, but there was negligible infiltration of neutrophils. These microglial cells expressed simultaneously growth regulated oncogene (Gro)-alpha and other ELR(+) CXC chemokines. Moreover, CD68-positive microglial cells also expressed the receptor for ELR(+) CXC chemokines. On day 4, capillary endothelial cells were significantly increased in the CA1 sector. Considering that ELR(+) CXC chemokines have potent angiogenic activities, the coordinate expression of ELR(+) CXC chemokines and their receptor CXCR2 in microglial cells may be related not only to the ischemic brain injuries but also to the microglial and capillary proliferation in the monkey hippocampus.
包括白细胞介素-8在内的E选择素配体阳性（ELR(+)）CXC趋化因子已知参与包括啮齿动物脑在内的各种器官的缺血再灌注损伤。然而，这些趋化因子在灵长类动物脑缺血再灌注损伤过程中的作用仍不清楚。在此，我们研究了CXC趋化因子及其受体CXCR2在猴海马体中的表达情况，已知该海马体在20分钟缺血和再灌注后第5天会出现整个CA1神经元丢失。在未缺血的猴子海马体中未检测到ELR(+)趋化因子及其受体CXCR2。相反，在再灌注开始后30 - 60分钟，海马体CA1区CD68阳性小胶质细胞显著增加，但中性粒细胞浸润可忽略不计。这些小胶质细胞同时表达生长调节致癌基因（Gro）-α和其他ELR(+) CXC趋化因子。此外，CD68阳性小胶质细胞也表达ELR(+) CXC趋化因子的受体。在第4天，CA1区的毛细血管内皮细胞显著增加。鉴于ELR(+) CXC趋化因子具有强大的血管生成活性，ELR(+) CXC趋化因子及其受体CXCR2在小胶质细胞中的协同表达可能不仅与缺血性脑损伤有关，还与猴海马体中的小胶质细胞和毛细血管增殖有关。
