中华航海医学与高气压医学杂志
中華航海醫學與高氣壓醫學雜誌
중화항해의학여고기압의학잡지
CHINESE JOURNAL OF NAUTICAL MEDICINE AND HYPERBARIC MEDICINE
2012年
6期
337-340,344
,共5页
季玉峰%周建光%方以群%周颖奇%刘长云
季玉峰%週建光%方以群%週穎奇%劉長雲
계옥봉%주건광%방이군%주영기%류장운
高压氧%急性脑创伤%含水量,血脑屏障%MMP-9%基因表达
高壓氧%急性腦創傷%含水量,血腦屏障%MMP-9%基因錶達
고압양%급성뇌창상%함수량,혈뇌병장%MMP-9%기인표체
Hyperbaric oxygen%Acute brain injury%Water content%Blood brain barrier%mutrix metallo proteinases 9%Gene expression
目的 观察高压氧(hyperbaric oxygen,HBO)治疗对急性脑创伤后血脑屏障损伤大鼠MMP-9 mRNA表达的影响,探讨高压氧治疗急性脑损伤的机制.方法 选取40只SD大鼠,采用自由落体打击法制备急性脑创伤模型.造模成功后采用数字表法随机分为4组,每组10只.分别为正常对照组:动物置于加压舱内,模拟除压力和氧浓度以外的其他实验条件.急性颅脑损伤24 h组:动物颅脑打击后1h,置于加压舱内,模拟除压力和氧浓度以外的其他实验条件,于伤后24 h断头取材.急性颅脑损伤高压氧治疗24h组:动物颅脑打击后1h和12 h,置于高压氧舱内,在0.25 MPa HBO下各停留40 min,于伤后24 h断头取材.急性颅脑损伤常氧高氮治疗24 h组:动物颅脑打击后1h和12 h,置于高压氧舱内,在0.25 MPa常氧高氮环境下各停留40 min,于伤后24 h 6只断头取材行含水量及RT-PCR测定,4只行脑组织伊文蓝(Evans blue,EB)测定.结果 急性颅脑损伤伤侧和非伤侧脑组织含水量为77.39 mg和72.25 mg,与急性颅脑损伤HBO治疗24 h组(70.83 mg、70.27 mg)比较差异有统计学意义(P＜0.05).急性颅脑损伤经0.25 MPa HBO治疗后,脑组织含水量较未治疗组下降(P＜0.01),高压氧治疗组半球及海马EB均显著增加(P＜0.05,P＜0.01).急性颅脑损伤经0.25 MPa HBO治疗后,损伤侧和非损伤侧半球及海马EB较未治疗组下降(P＜0.0,1),急性颅脑损伤组及0.25 MPa常氧高氮组损伤侧半球及海马EB多于非损伤侧(P＜0.05),0.25 MPa HBO治疗组损伤侧半球及海马EB高于非损伤侧(P＜0.05).急性颅脑损伤经0.25 MPa HBO治疗后,损伤侧和非损伤侧半球及海马MMP-9 mRNA较未治疗组下降(P＜0.0,1).急性颅脑损伤组、0.25 MPa常氧高氮组及0.25 MPa HBO治疗组损伤侧半球及海马MMP-9mRNA高于非损伤侧(均P＜0.05).结论 HBO治疗急性脑创伤可以保护血脑屏障,从而减轻脑水肿,机制之一是HBO治疗减少了MMP-9 mRNA表达.
目的 觀察高壓氧(hyperbaric oxygen,HBO)治療對急性腦創傷後血腦屏障損傷大鼠MMP-9 mRNA錶達的影響,探討高壓氧治療急性腦損傷的機製.方法 選取40隻SD大鼠,採用自由落體打擊法製備急性腦創傷模型.造模成功後採用數字錶法隨機分為4組,每組10隻.分彆為正常對照組:動物置于加壓艙內,模擬除壓力和氧濃度以外的其他實驗條件.急性顱腦損傷24 h組:動物顱腦打擊後1h,置于加壓艙內,模擬除壓力和氧濃度以外的其他實驗條件,于傷後24 h斷頭取材.急性顱腦損傷高壓氧治療24h組:動物顱腦打擊後1h和12 h,置于高壓氧艙內,在0.25 MPa HBO下各停留40 min,于傷後24 h斷頭取材.急性顱腦損傷常氧高氮治療24 h組:動物顱腦打擊後1h和12 h,置于高壓氧艙內,在0.25 MPa常氧高氮環境下各停留40 min,于傷後24 h 6隻斷頭取材行含水量及RT-PCR測定,4隻行腦組織伊文藍(Evans blue,EB)測定.結果 急性顱腦損傷傷側和非傷側腦組織含水量為77.39 mg和72.25 mg,與急性顱腦損傷HBO治療24 h組(70.83 mg、70.27 mg)比較差異有統計學意義(P＜0.05).急性顱腦損傷經0.25 MPa HBO治療後,腦組織含水量較未治療組下降(P＜0.01),高壓氧治療組半毬及海馬EB均顯著增加(P＜0.05,P＜0.01).急性顱腦損傷經0.25 MPa HBO治療後,損傷側和非損傷側半毬及海馬EB較未治療組下降(P＜0.0,1),急性顱腦損傷組及0.25 MPa常氧高氮組損傷側半毬及海馬EB多于非損傷側(P＜0.05),0.25 MPa HBO治療組損傷側半毬及海馬EB高于非損傷側(P＜0.05).急性顱腦損傷經0.25 MPa HBO治療後,損傷側和非損傷側半毬及海馬MMP-9 mRNA較未治療組下降(P＜0.0,1).急性顱腦損傷組、0.25 MPa常氧高氮組及0.25 MPa HBO治療組損傷側半毬及海馬MMP-9mRNA高于非損傷側(均P＜0.05).結論 HBO治療急性腦創傷可以保護血腦屏障,從而減輕腦水腫,機製之一是HBO治療減少瞭MMP-9 mRNA錶達.
목적 관찰고압양(hyperbaric oxygen,HBO)치료대급성뇌창상후혈뇌병장손상대서MMP-9 mRNA표체적영향,탐토고압양치료급성뇌손상적궤제.방법 선취40지SD대서,채용자유락체타격법제비급성뇌창상모형.조모성공후채용수자표법수궤분위4조,매조10지.분별위정상대조조:동물치우가압창내,모의제압력화양농도이외적기타실험조건.급성로뇌손상24 h조:동물로뇌타격후1h,치우가압창내,모의제압력화양농도이외적기타실험조건,우상후24 h단두취재.급성로뇌손상고압양치료24h조:동물로뇌타격후1h화12 h,치우고압양창내,재0.25 MPa HBO하각정류40 min,우상후24 h단두취재.급성로뇌손상상양고담치료24 h조:동물로뇌타격후1h화12 h,치우고압양창내,재0.25 MPa상양고담배경하각정류40 min,우상후24 h 6지단두취재행함수량급RT-PCR측정,4지행뇌조직이문람(Evans blue,EB)측정.결과 급성로뇌손상상측화비상측뇌조직함수량위77.39 mg화72.25 mg,여급성로뇌손상HBO치료24 h조(70.83 mg、70.27 mg)비교차이유통계학의의(P＜0.05).급성로뇌손상경0.25 MPa HBO치료후,뇌조직함수량교미치료조하강(P＜0.01),고압양치료조반구급해마EB균현저증가(P＜0.05,P＜0.01).급성로뇌손상경0.25 MPa HBO치료후,손상측화비손상측반구급해마EB교미치료조하강(P＜0.0,1),급성로뇌손상조급0.25 MPa상양고담조손상측반구급해마EB다우비손상측(P＜0.05),0.25 MPa HBO치료조손상측반구급해마EB고우비손상측(P＜0.05).급성로뇌손상경0.25 MPa HBO치료후,손상측화비손상측반구급해마MMP-9 mRNA교미치료조하강(P＜0.0,1).급성로뇌손상조、0.25 MPa상양고담조급0.25 MPa HBO치료조손상측반구급해마MMP-9mRNA고우비손상측(균P＜0.05).결론 HBO치료급성뇌창상가이보호혈뇌병장,종이감경뇌수종,궤제지일시HBO치료감소료MMP-9 mRNA표체.
Objective To observe effects of hyperbaric oxygen (HBO) on blood-brain barrier and the expression of MMP-9 mRNA following acute brain injury (ABI) and also to explore the mechanism involved in the treatment of ABI.Methods Forty SD rats were selected for the experiment.Following development of the ABI model by using free-fall hit method,the animals were randomly divided into 4 groups:the normal control group,the 24 h ABI group,the 24 h HBO therapy group and the 24 h normoxic nitrogen rich therapy group,each consisting of 10 animals.(1) The animals in the normal control group were simply housed in the chamber and received all the same treatments,except for high pressure and high level of oxygen breathing.(2) One hour after ABI,the animals in the 24 h ABI group were put into the hyperbaric chamber and received all the same treatments except for high pressure and high level of oxygen breathing,then they were killed 24 h after injury for collection of samples.(3) The animals in the ABI and 24 h HBO therapy groups were also housed in the hyperbaric chamber 1 h and 12 h after brain injury,and stayed at 0.25 MPa for a duration of 40 min,then they were sacrificed 24 h after injury.(4) The animals in the 24 h normoxic nitrogen rich therapy group were exposed to the 0.25 MPa normoxic nitrogen rich environment for a duration of 40 min,1 h and 12 h after brain injury,then 6 of the animals were killed 24 h after injury for the measurement of water content and RT-PCR,and 4 of the animals were killed for Evans blue detection (EB).Results Water contents both in the injured side and non-injured side of the brain following acute brain injury were 77.39 mg and 72.25 mg respectively,and statistical significance could be noticed when compared with the 24 h HBO therapy group(70.83 mg、70.27 mg) (P ＜ 0.05).Following 0.25 MPa HBO treatment of ABI,water content of the brain tissue decreased when compared with that of the non-treatment group (water contents of the brain tissue were 70.83 for the injured side and 77.39 for the non-injured side,P ＜0.01).Changes in brain tissue EB after HBO treatment were as follows:EB increased significantly both in the injured side and non-injured side of the hemisphere,and the hippocampus,following ABI and various treatments (P ＜ 0.05,P ＜0.01).As shown in the study,EB in the injured side and non-injured side of the hemisphere and the hippocampus decreased,when compared with those of the non-treatment group,following 0.25 MPa HBO therapy (P ＜ 0.01).Changes in the expression of MMP-9 mRNA were as follows:the expression of MMP-9 mRNA in the injured side and non-injured side of the hemisphere and hippocampus all increased significantly,following ABI and various treatment (P ＜ 0.05,P ＜0.01).After 0.25 MPa HBO treatment of ABI,the expression of MMP-9 mRNA in the injured side and non-injured side of the hemisphere and hippocampus decreased,when compared with that of the non-treatment group (P ＜ 0.01).Conclusions HBO treatment of ABI could protect the blood-brain barrier,thus alleviating cerebral edema.One of the mechanisms involved might be the reduction in the expression of MMP-9 mRNA through HBO treatment.
