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系统观察大鼠ＣＮＳ针刺损伤后表达ｂＦＧＦ、ＦＧＦ受体（ＦＧＦＲ）和ＧＦＡＰ的细胞种类、时相以及相互影响，探讨ＦＧＦＲ抑制剂——５′－ＭＴＡ对体内反应性星形胶质化的影响。将７５ 只ＳＤ雄性大鼠均分１５ 组：伤后０．５ ｈ～３０ ｄ 处死的实验组与对照组。将２０ 只雄性Ｗｉｓｔａｒ大鼠均分２ 大组。甲组伤后４ ｄ 处死（５ 只加药鼠），乙组伤后８ ｄ 处死（５ 只加药鼠）；其中非加药鼠作相应单纯损伤对照组。ＨＥ染色和免疫组化染色观测ｂＦＧＦ、ＦＧＦＲ和ＧＦＡＰ表达并作形态定量分析。伤后０．５ ｈ，星形胶质细胞（Ａｓ）胞核肿胀；尔后伤道周围神经元脱失；４ ｄ 起受损组织渐为反应性Ａｓ填补；ＧＦＡＰ反应于４～７ ｄ 达顶峰。４～６ ｈ，Ａｓ 和神经元表达ｂＦＧＦ先后增强；２～４ ｄ，脑内ｂＦＧＦ水平最高，以Ａｓ为主；核仁ｂＦＧＦ亦为阳性。１２ ｈ，ＦＧＦＲ表达轻度增强，１ ｄ 时达高峰，随即回落。５′－ＭＴＡ加药组，４ ｄ 时伤区细胞数量及ｂＦＧＦ和ＧＦＡＰ表达强度均低于对照组；加药组伤道（８ ｄ）明显宽于对照组。提示：脑损伤后Ａｓ首先反应性表达ｂＦＧＦ，Ａｓ 自分泌ｂＦＧＦ是反应性星形胶质化的主要始动机制。ｂＦＧＦ可能内化入核仁发挥效应。伤?
To observe the cell type, phase and interaction of bFGF, FGFR and GFAP after rat CNS acupuncture injury, to investigate the effect of FGFR inhibitor-5’-MTA on in vivo reactive astrogliosis influences. Fifty-five male Sprague-Dawley rats were equally divided into 15 groups: the experimental group and the control group which were sacrificed from 0.5 h to 30 d after injury. Twenty male Wistar rats were divided into two groups. Group A was sacrificed 4 d after injury (5 dosing mice), group B was sacrificed 8 d after injury (5 dosing mice); The expression of bFGF, FGFR and GFAP was observed by HE staining and immunohistochemistry, and the morphology was quantitatively analyzed. 0.5 h after injury, astrocytes (As) nuclei were swollen; after injury, the peripheral neurons were lost; damaged tissue gradually became reactive As filling 4 days after injury; GFAP reached its peak at 4 ~ 7 days . From 4 h to 6 h, bFGF increased in As and neurons. The level of bFGF in the brain was the highest at 2 to 4 days, and As was the main factor. The nucleolus bFGF was also positive. At 12 h, the expression of FGFR increased slightly, reaching its peak on the 1st day and then dropped back. The number of cells in the injured area and the expression of bFGF and GFAP in the 5’-MTA dosing group were lower than those in the control group on the 4th day. The injury pathways in the dosing group were significantly wider than those in the control group. It is suggested that AS first reacts with bFGF and AS autocrine bFGF after brain injury is the main initiating mechanism of reactive astrogliosis. bFGF may internalize into the nucleolus to exert an effect. hurt?