成年大鼠持续性脑缺血后TGFβ1蛋白表达与凋亡的关系

摘要

Objective：To observe the change of TGFβ1 protein and the relationship between the expression of TGFβ1 protein and neuron apoptosis in adult rats following permanent middle cerebral artery occlusion. Methods: The rat model of focal cerebral ischemia was established by permanent middle cerebral occlusion. One hour after ischemia, the experiental groups were treated with dexamethasone(5mg/kg) while the control groups were treated with saline. Immunohistochemistry and Tunel methods were used to show the expression of TGFβ1 protein and apoptosis. Results: The expression time-course of TGFβ1 protein was two-phase. The first peak of expression was at 6h; the second was from 24h to 72h. The TUNEL-positive apoptotic cells were present from 24h to 5d, localizing at the border zone of infarct. The significant decrease in expression of TGFβ1 protein and significant increase of the number of TUNEL-positive apoptotic cells in rats treated with dexamethasone was observed compared with that of control group. Conclusion: TGFβ1 protein may antagonize the neuron apoptosis after permanent focal cerebral ischmia%目的：观察成年大鼠持续性局灶脑缺血后TGFβ1蛋白表达与缺血后凋亡的关系。方法：单侧大脑中动脉近端电凝术建立大鼠持续性局灶脑缺血模型。缺血后1h，实验组经尾静脉注射氟美松(5mg/kg)，对照组注射相同容积的生理盐水。缺血后3h～120h取材，分别用免疫组织化学SP法和原位末端标记TUNEL法标记TGFβ1蛋白表达细胞和凋亡细胞。结果：持续性局灶脑缺血后TGFβ1蛋白呈双相性，主要分布在梗塞灶周围区域。 TGFβ1的表达可被氟美松抑制，同时缺血后神经细胞凋亡也加重。结论：大鼠持续性局灶脑缺血后梗塞灶周围区域TGFβ1蛋白表达可能有减轻缺血后神经细胞凋亡的作用。