CELL-PROLIFERATION AFTER ISCHEMIC-INJURY IN GERBIL BRAIN - AN IMMUNOCYTOCHEMICAL AND AUTORADIOGRAPHIC STUDY
CELL-PROLIFERATION AFTER ISCHEMIC-INJURY IN GERBIL BRAIN - AN IMMUNOCYTOCHEMICAL AND AUTORADIOGRAPHIC STUDY
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DOI：
10.1007/bf00225558
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发表时间：
1985-01-01
影响因子：
3.6
通讯作者：
GOLDSTEIN, GW
中科院分区：
文献类型：
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作者：
DUBOIS, M;BOWMAN, PD;GOLDSTEIN, GW
用氚标记胸腺嘧啶核苷放射自显影技术观察沙土鼠脑缺血损伤后细胞增殖情况。沙鼠的颈总动脉的双侧闭塞，导致在后丘脑或中脑的坏死，或梗死区。缺血12 h ~ 10 d，注射3 H-TdR，4 h后处死，取脑切片。为了识别星形胶质细胞和单核细胞/巨噬细胞，免疫细胞化学进行放射自显影之前，使用抗血清对胶质细胞酸性蛋白和内皮单核细胞网状内皮抗原，分别。免疫细胞化学也被用来可视化微血管层粘连蛋白，髓鞘，和泄漏的血清白蛋白。最后，采用酸性磷酸酶活性的组织化学方法来验证伤口中的细胞吞噬活性。在缺血后的前10天内发生了一系列可重复的反应。早期变化包括白蛋白渗漏和髓磷脂分解，随后在2天时单核细胞到达，并在5天时分化为巨噬细胞。这些细胞在缺血后2 - 6天表现出强烈的增殖。微血管内皮细胞在缺血后4天最大标记。肥大的星形胶质细胞在缺血后2天明显，并在缺血后3 - 7天增殖，到10天，伤口被“胶质瘢痕”取代。
Tritiated thymidine autoradiography was used to measure cellular proliferation after ischemic injury in gerbil brain. Gerbils were subjected to bilateral occlusion of the common carotid arteries which resulted in areas of necrosis, or infarcts, in the posterior thalamus or midbrain. From 12 h to 10 days following the ischemia, gerbils were injected with3H thymidine, sacrificed 4 h later, and the brains sectioned. In order to identify astrocytes and monocytes/macrophages, immunocytochemistry was performed prior to autoradiography, using antisera against glial fibrillary acidic protein and endothelial-monocyte reticuloendothelial antigen, respectively. Immunocytochemistry was also used to visualize microvessel laminin, myelin, and leakage of serum albumin. Lastly, a histochemical procedure for acid phosphatase activity was employed to verify cellular phagocytic activity in the wound. A reproducible sequence of reactions took place during the first 10 days after ischemia. Early changes included leakage of albumin and myelin breakdown, followed by arrival of monocytes at 2 days and their differentiation into macrophages by 5 days. These cells exhibited intense proliferation from 2 to 6 days post-ischemia. Microvessel endothelial cells were maximally labeled at 4 days post-ischemia. Hypertrophied astrocytes were apparent at 2 days and proliferated from 3 to 7 days post-ischemia, and by 10 days the wound was replaced by a “glial scar”.