中文摘要：

目的观察高压氧（HBO）治疗对大鼠大脑皮质损伤后胶质疤痕形成的影响，并初步探讨其对炎性反应产生抑制作用的内在作用机制。方法选取健康成年雄性SD大鼠96只，建立大脑穿刺损伤模型，采用随机数字表法将其分为对照组和治疗组，每组48只，对照组不做特殊干预处理，治疗组则给予HBO治疗。分别于脑穿刺损伤后1、3、7、14和28d取大鼠右侧大脑组织，利用免疫组化染色比较2组大鼠损伤灶周围星形胶质细胞和小胶质细胞的数目变化，并通过ELISA法测定脑组织内肿瘤坏死因子α（TNF-α）、白细胞介素1β（IL-1β）的含量。结果制模后7、14和28d，对照组大鼠的伤口面积分别为（2．73±0．05）μm^2、（3．42±0．18）μm^2、（2．41±0．09）μm^2，与制模后7d及14d比较，制模后28d时的伤口面积明显缩小（P〈0．05）；治疗组大鼠制模后7、14和28d的伤口面积分别为（2．78±0．12）μm^2、（2．59±0．08）μm^2、（1．20±0．06）μm^2，与制模后7d比较，制模后14d时的伤口面积缩小（P〈0．05），且制模后28d时的伤口面积进一步缩小（P〈0．05），制模后14d及28d时的伤口面积均小于对照组（P〈0．05）。与制模后7d比较，对照组及治疗组制模后14d和28d的星形胶质细胞数目均增多（P〉0．05）；与组内制模后14d比较，对照组及治疗组制模后28d的星形胶质细胞数目下降（P〈0．05）；与对照组同时间点比较，治疗组星形胶质细胞的数目少于对照组（P〈0．05）。与制模后1d比较，对照组及治疗组制模后3d、7d的小胶质细胞均增多（P〉0．05）；与组内制模后7d比较，对照组及治疗组制模后14d的小胶质细胞数目下降（P〈0．05）；与对照组同时间点比较，治疗组小胶质细胞的数目少于对照组（P〈0．05）。与制模后1d比较，对照组制模后3d及7d的TNF-α浓度均较高（P〉0．05），但制模后

英文摘要：

Objective To observe any influence of hyperbaric oxygen （HBO） treatment on the formation of glial scars, and to explore how HBO suppresses the inflammatory reaction to injury. Methods A total of 96 healthy, adult, male, Sprague-Dawley rats were used to model cerebral puncture injury. They were then randomized into a control group and a treatment group, with 48 rats in each group. The treatment group received HBO treatment, while the control group received no special treatment. At 1 , 3, 7, 14 and 28 days after the puncture injury, the rats＇ right brain tissues were harvested and immunohistochemical staining was employed to compare the changes in number of astrocytes and microglial cells around the injury in the two groups. The level of tumor necrosis factor α （TNF-α） and interleukin 1β （IL-1β） in the cerebral tissue was examined using ELISA. Results Among the control group the average wound areas after 7, 14 and 28 days were （2.73 ±0.05）μm2, （3.42±0.18）μm2 and （2.41 ±0.09） μm2 , a significant reduction after 28 days compared with 7 and 14 days. The corresponding average wound areas of rats in the treatment group were （2.78 ± 0.12） μm2 , （2.59 ± 0.08 ） μm2 and （ 1.20 ± 0.06 ） μm2. There the aver-age wound area had decreased significantly after 14 days, and the further reduction after 28 days was also significant. The numbers of GFAP-positive astrocytes at 14 and 28 days had increased significantly compared with after 7 days in both the control group and the treatment group. The average number of GFAP-positive astrocytes in the control group at 28 days had decreased significantly compared with after 14 days. Compared with the control group at the same time points, the number of GFAP-positive astrocytes in the treatment group was significantly less. After modeling, the number of ionized calcium-binding adapter molecule 1 （Ibal）-positive microglial ceils increased significantly, but there was a significant decrease in both the control and treatment groups by 7