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用鼠脑星形胶质细胞（ＡＳ）原代培养技术建立体外ＡＳ机械性损伤模型。以ｃ—Ｆｏｘｓ、ｂＦＧＦ、ＰＣＮＡ、ＧＦＡＰ—ｍＲＮＡ、ＧＦＡＰ和Ｍｙｏｓｉｎ作为观察指标研究反应性星形胶质化的形成机制。结果显示：１．ｃ—Ｆｏｓ蛋白于损伤后４５ｍｉｎ即有阳性表达，伤后２ｈ消失；２．损伤后２ｈ，损伤边缘的ＡＳ开始表达ｂＦＧＦ，１２ｈ达高峰，２ｄ后表达强度开始回落；３．损伤边缘的部分ＡＳ于损伤后２ｈ开始表达ＰＣＮＡ，伤后１ｄ，ＰＣＮＡ阳性的ＡＳ沿损伤边缘呈列兵式整齐排列，２ｄ后ＰＣＮＡ阳性的ＡＳ分布于损伤周围区域；４．损伤后４ｈ，损伤边缘的ＡＳ开始表达Ｍｙｏｓｉｎ，并逐渐增加，而且朝向损伤区胞浆突起的阳性表达强于背向损伤区的突起；５．损伤边缘的ＡＳ于损伤后６ｈ开始表达ＧＦＡＰ—ｍＲＮＡ，１ｄ达高峰，２ｄ开始回落，３ｄ则只在少数ＡＳ中可检出ＧＦＡＰ—ｍＲＮＡ；６．损伤后１ｄ，ＧＦＡＰ表达明显增强，胞体肥大并向损伤区伸出粗大突起，２ｄＧＦＡＰ达高峰，３ｄ肥大ＡＳ的胞体和突起覆盖损伤区；７．在体外ＡＳ机械性损伤模型上，在没有神经元和其它复杂因素影响的条件下，ＡＳ对损伤的主要反应是胞体的肥大、突起的粗大，并能独立形成反应性星形胶质化。
In vitro AS mechanical injury model was established by primary culture of mouse astrocytes (AS). The formation mechanism of reactive astrogliosis was investigated using c-Foxs, bFGF, PCNA, GFAP-mRNA, GFAP and Myosin as the observation indexes. The result shows: 1. The expression of c-Fos protein was positive at 45 min after injury and disappeared at 2 h after injury. At 2h after injury, bFGF began to be expressed in the margins of the lesion, reached the peak at 12h, and then began to drop after 2 days. 3. The AS of injury margin began to express PCNA at 2h after injury. On the 1st day after injury, PCNA positive AS was aligned along the injury margin, and PCNA positive AS distributed 2 weeks after injury. At 4h after injury, Myosin began to be expressed at the marginal edge of the lesion, and gradually increased. The positive expression of cytoplasmic protrusions toward the lesion was stronger than that of the dorsal to the lesion. The expression of GFAP-mRNA began to be detected at 6h after injury, and reached the peak on the 1st day and began to decline on the 2nd day. The GFAP-mRNA was detected only in a few AS on the 3rd day. On the 1st day after injury, the expression of GFAP was significantly increased, the somatic cell hypertrophy and large protrusions protruding to the injury area, reaching the peak at 2dGFAP, and the cell bodies and protrusions of 3d hypertrophy covered the injury area. AS mechanical injury in vitro model, in the absence of neurons and other complex factors under the conditions of AS, the main response to damage is the cell body hypertrophy, protruding thick, and can form a separate reactive astrogliosis.