高压氧治疗对大鼠脑穿刺损伤后胶质疤痕形成和炎性反应的抑制作用
고압양치료대대서뇌천자손상후효질파흔형성화염성반응적억제작용
Hyperbaric oxygen for suppressing glial scar formation and inflammation after a stab wound to the cerebral cortex
  • 万方数据
    中华物理医学与康复杂志 중화물리의학여강복잡지
    CHINESE JOURNAL OF PHYSICAL MEDICINE AND REHABILITATION
    2013年 6期 442-446 ,共5页

    尹娜%王玉%韩远远%贺慧艳%左健

    윤나%왕옥%한원원%하혜염%좌건

    高压氧%胶质疤痕%小胶质细胞%星形胶质细胞%炎性细胞因子 高壓氧%膠質疤痕%小膠質細胞%星形膠質細胞%炎性細胞因子
    고압양%효질파흔%소효질세포%성형효질세포%염성세포인자
    Hyperbaric oxygen%Glial scars%Microglia%Astrocytes%Inflammatory cytokines
    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28 d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28 d,对照组大鼠的伤口面积分别为(2.73±0.05) μm2、(3.42±0.18)μm 2、(2.41±0.09) μm2,与制模后7d及14 d比较,制模后28 d时的伤口面积明显缩小(P＜0.05)；治疗组大鼠制模后7、14和28 d的伤口面积分别为(2.78 ±0.12)μm2、(2.59±0.08) μm2、(1.20±0.06) μm2,与制模后7d比较,制模后14 d时的伤口面积缩小(P＜0.05),且制模后28 d时的伤口面积进一步缩小(P＜0.05),制模后14 d及28 d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14 d和28 d的星形胶质细胞数目均增多(P＞0.05)；与组内制模后14 d比较,对照组及治疗组制模后28 d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14 d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7d的TNF-α浓度较制模后3d低(P＜0.05)；制模后3d及7d,对照组IL-1β浓度和治疗组TNF-α浓度均呈先升高后降低趋势；治疗组IL-1β浓度则呈逐渐降低趋势(P＜0.05).与对照组同时间点比较,治疗组TNF-α浓度及IL-1β浓度均较低(P＜0.05).结论 HBO治疗可促进脑穿刺损伤伤口愈合,减少胶质疤痕形成,其机制可能与星形胶质细胞及小胶质细胞活化水平下调、参与炎性反应的细胞因子含量减少有关.
    목적 관찰고압양(HBO)치료대대서대뇌피질손상후효질파흔형성적영향,병초보탐토기대염성반응산생억제작용적내재작용궤제.방법 선취건강성년웅성SD대서96지,건립대뇌천자손상모형,채용수궤수자표법장기분위대조조화치료조,매조48지,대조조불주특수간예처리,치료조칙급여HBO치료.분별우뇌천자손상후1、3、7、14화28 d취대서우측대뇌조직,이용면역조화염색비교2조대서손상조주위성형효질세포화소효질세포적수목변화,병통과ELISA법측정뇌조직내종류배사인자α(TNF-α)、백세포개소1β(IL-1β)적함량.결과 제모후7、14화28 d,대조조대서적상구면적분별위(2.73±0.05) μm2、(3.42±0.18)μm 2、(2.41±0.09) μm2,여제모후7d급14 d비교,제모후28 d시적상구면적명현축소(P＜0.05)；치료조대서제모후7、14화28 d적상구면적분별위(2.78 ±0.12)μm2、(2.59±0.08) μm2、(1.20±0.06) μm2,여제모후7d비교,제모후14 d시적상구면적축소(P＜0.05),차제모후28 d시적상구면적진일보축소(P＜0.05),제모후14 d급28 d시적상구면적균소우대조조(P＜0.05).여제모후7d비교,대조조급치료조제모후14 d화28 d적성형효질세포수목균증다(P＞0.05)；여조내제모후14 d비교,대조조급치료조제모후28 d적성형효질세포수목하강(P＜0.05)；여대조조동시간점비교,치료조성형효질세포적수목소우대조조(P＜0.05).여제모후1d비교,대조조급치료조제모후3d、7d적소효질세포균증다(P＞0.05)；여조내제모후7d비교,대조조급치료조제모후14 d적소효질세포수목하강(P＜0.05)；여대조조동시간점비교,치료조소효질세포적수목소우대조조(P＜0.05).여제모후1d비교,대조조제모후3d급7d적TNF-α농도균교고(P＞0.05),단제모후7d적TNF-α농도교제모후3d저(P＜0.05)；제모후3d급7d,대조조IL-1β농도화치료조TNF-α농도균정선승고후강저추세；치료조IL-1β농도칙정축점강저추세(P＜0.05).여대조조동시간점비교,치료조TNF-α농도급IL-1β농도균교저(P＜0.05).결론 HBO치료가촉진뇌천자손상상구유합,감소효질파흔형성,기궤제가능여성형효질세포급소효질세포활화수평하조、삼여염성반응적세포인자함량감소유관.
    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 1 β (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 average 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-positivc astrocytes in the treatment group was significantly less.After modeling,the number of ionized calcium-binding adapter molecule Ⅰ (Ibal)-positive microglial cells increased significantly,but there was a significant decrease in both the control and treatment groups by 7 days.The average number of Ibal-positive microglial cells in the treatment group was significantly less than in the control group at all of the time points.Compared with the first day after modeling,the TNF-α concentration of the controls at 3 and 7 days was significantly higher,but by the 7th day it was significantly lower than it had been after 3 days.The average IL-1β concentration in the control group and TNF-α concentration in the treatment group had increased by day 3,but then decreased by day 7.The IL-1β concentration of the treatment group declined gradually.The average TNF-α and IL-1 β concentrations of the treatment group were significantly lower than those of the control group at all of the time points.Conclusion HBO treatment has a relatively good curative effect on cerebral puncture injury.It can accelerate wound healing and reduce the formation of glial scars.Its mechanism could be related to the deactivation of astrocytes and microglia cells and reducing the levels of cell factors that promote inflammation.
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