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目的探讨粒细胞集落刺激因子(G-CSF)对大鼠局灶性脑缺血的疗效及其相关机制。方法采用改良线栓法建立永久性局灶性大脑中动脉闭塞(MCAO)模型大鼠12只,并随机分为2组,G-CSF组术后2h用G-CSF行皮下注射干预,对照组行PBS干预,采用t检验比较组间术后24h脑梗死灶的体积差异(TTC染色法)和炎症及趋化因子TNF-α、TGF-β、IL-10、MCP-1 mRNA水平(RT-PCR法)和CD11b分子的表达(免疫组织化学染色法)水平差异。结果 G-CSF组比对照组梗死体积减小19.6%(P=0.001);G-CSF组MCP-1mRNA水平较对照组减少约22%(P=0.03),G-CSF组IL-10mRNA水平较对照组增高47%(P=0.01),而TGF-βmRNA则较对照组增高约1倍(P<0.01),但TNF-αmRNA水平在2组间无明显差异(P=0.88);G-CSF组与对照组缺血区域的CD11b浸润数目无明显差异(P=0.61)。结论 G-CSF能显著减少局灶性脑缺血的梗死体积,机制可能涉及TGF-β、IL-10、MCP-1等一系列重要的炎症和趋化因子。
Objective To investigate the efficacy and mechanism of granulocyte-colony stimulating factor (G-CSF) on focal cerebral ischemia in rats. Methods Twelve permanent focal middle cerebral artery occlusion (MCAO) rats were established by modified suture method and randomly divided into two groups. The G-CSF group was subcutaneously injected with G-CSF 2h after operation, while the control group The levels of inflammatory and chemokines TNF-α, TGF-β, IL-10 and MCP-1 mRNA (RT-PCR) PCR) and CD11b expression (immunohistochemical staining) level differences. Results The infarct volume in G-CSF group was decreased by 19.6% (P = 0.001). The level of MCP-1 mRNA in G-CSF group was decreased by about 22% (P = 0.03) The level of TGF-βmRNA increased by 47% (P = 0.01) in the control group and TGF-βmRNA increased by about 1 time compared with the control group (P <0.01) There was no significant difference in the number of CD11b infiltration between ischemic and control groups (P = 0.61). Conclusion G-CSF can significantly reduce the infarct volume after focal cerebral ischemia. The mechanism may involve a series of important inflammation and chemokines such as TGF-β, IL-10 and MCP-1.