中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2014年
1期
34-38
,共5页
施振华%裘五四%王卫民%姜启周%秦智勇
施振華%裘五四%王衛民%薑啟週%秦智勇
시진화%구오사%왕위민%강계주%진지용
高压氧%预处理%大鼠%脑出血%脑水肿%血红素加氧酶-1%锌原卟啉Ⅸ
高壓氧%預處理%大鼠%腦齣血%腦水腫%血紅素加氧酶-1%鋅原卟啉Ⅸ
고압양%예처리%대서%뇌출혈%뇌수종%혈홍소가양매-1%자원계람Ⅸ
Hyperbaric oxygen%Preconditioning%Rat%Intracerebral hemorrhage%Brain edema%Heme oxygenase-1%Zinc protoporphyrin
目的 研究血红素加氧酶-1(heme oxygenase-1,HO-1)在高压氧预处理(hyperbaic oxygen preconditioning,HBOP)减轻大鼠脑出血后脑水肿形成过程中的作用.方法 本实验共选用54只雄性Spradgue-Dawley大鼠,体质量300～ 350 g,分为两部分:第1部分,6只大鼠随机(随机数字法)分为两组(n=3),分别接受高压氧预处理(HBOP组)或假预处理(假预处理组);预处理结束24 h后处死,取基底节组织,采用Western blot法检测HO-1蛋白含量.第2部分:48只SD大鼠随机(随机数字法)分为四组(n=12),各组大鼠在预处理前腹腔内置入含HO-1抑制剂锌原卟啉Ⅸ(zinc protoporphyrinⅨ,ZnPPⅨ)的缓泵(0.01mg/kg)(HBOP+ ZnPP组、假预处理+ ZnPP组)或含2 mL二甲基亚砜(dimethyl sulfoxide,DMSO)载体溶剂的缓释泵作为对照(HBOP+ DMSO组、假预处理+DMSO组),随后接受高压氧预处理(HBOP组+ZnPP组,HBOP+DMSO组)或假预处理(假预处理+ZnPP组,假预处理+DMSO组).预处理结束24h后,立体定向基底节内注射自体股动脉血100 μL建立基底节脑出血模型,72 h后处死,采用干湿质量法测定脑组织水含量.统计学分析采用Stata 7.0软件进行成组设计资料的t检验.结果 HBOP组大鼠基底节组织内HO-1蛋白含量与假预处理相比差异具有统计学意义(P＜0.05);HBOP+ DMSO组大鼠血肿同侧基底节组织水含量为(81.4±0.9)％,显著低于假预处理+ DMSO组(82.6±0.8)％(P＜0.05),但大鼠接受高压氧预处理同时腹腔内给予HO-1抑制剂ZnPPⅨ则抵消了HBOP减轻脑出血后脑水肿的效应[(82.8±0.9)％vs.(82.6±0.7)％(P＞0.05)].结论 高压氧预处理显著减轻大鼠脑出血后脑水肿,其作用机制与其上调HO-1蛋白的表达有关.
目的 研究血紅素加氧酶-1(heme oxygenase-1,HO-1)在高壓氧預處理(hyperbaic oxygen preconditioning,HBOP)減輕大鼠腦齣血後腦水腫形成過程中的作用.方法 本實驗共選用54隻雄性Spradgue-Dawley大鼠,體質量300～ 350 g,分為兩部分:第1部分,6隻大鼠隨機(隨機數字法)分為兩組(n=3),分彆接受高壓氧預處理(HBOP組)或假預處理(假預處理組);預處理結束24 h後處死,取基底節組織,採用Western blot法檢測HO-1蛋白含量.第2部分:48隻SD大鼠隨機(隨機數字法)分為四組(n=12),各組大鼠在預處理前腹腔內置入含HO-1抑製劑鋅原卟啉Ⅸ(zinc protoporphyrinⅨ,ZnPPⅨ)的緩泵(0.01mg/kg)(HBOP+ ZnPP組、假預處理+ ZnPP組)或含2 mL二甲基亞砜(dimethyl sulfoxide,DMSO)載體溶劑的緩釋泵作為對照(HBOP+ DMSO組、假預處理+DMSO組),隨後接受高壓氧預處理(HBOP組+ZnPP組,HBOP+DMSO組)或假預處理(假預處理+ZnPP組,假預處理+DMSO組).預處理結束24h後,立體定嚮基底節內註射自體股動脈血100 μL建立基底節腦齣血模型,72 h後處死,採用榦濕質量法測定腦組織水含量.統計學分析採用Stata 7.0軟件進行成組設計資料的t檢驗.結果 HBOP組大鼠基底節組織內HO-1蛋白含量與假預處理相比差異具有統計學意義(P＜0.05);HBOP+ DMSO組大鼠血腫同側基底節組織水含量為(81.4±0.9)％,顯著低于假預處理+ DMSO組(82.6±0.8)％(P＜0.05),但大鼠接受高壓氧預處理同時腹腔內給予HO-1抑製劑ZnPPⅨ則牴消瞭HBOP減輕腦齣血後腦水腫的效應[(82.8±0.9)％vs.(82.6±0.7)％(P＞0.05)].結論 高壓氧預處理顯著減輕大鼠腦齣血後腦水腫,其作用機製與其上調HO-1蛋白的錶達有關.
목적 연구혈홍소가양매-1(heme oxygenase-1,HO-1)재고압양예처리(hyperbaic oxygen preconditioning,HBOP)감경대서뇌출혈후뇌수종형성과정중적작용.방법 본실험공선용54지웅성Spradgue-Dawley대서,체질량300～ 350 g,분위량부분:제1부분,6지대서수궤(수궤수자법)분위량조(n=3),분별접수고압양예처리(HBOP조)혹가예처리(가예처리조);예처리결속24 h후처사,취기저절조직,채용Western blot법검측HO-1단백함량.제2부분:48지SD대서수궤(수궤수자법)분위사조(n=12),각조대서재예처리전복강내치입함HO-1억제제자원계람Ⅸ(zinc protoporphyrinⅨ,ZnPPⅨ)적완빙(0.01mg/kg)(HBOP+ ZnPP조、가예처리+ ZnPP조)혹함2 mL이갑기아풍(dimethyl sulfoxide,DMSO)재체용제적완석빙작위대조(HBOP+ DMSO조、가예처리+DMSO조),수후접수고압양예처리(HBOP조+ZnPP조,HBOP+DMSO조)혹가예처리(가예처리+ZnPP조,가예처리+DMSO조).예처리결속24h후,입체정향기저절내주사자체고동맥혈100 μL건립기저절뇌출혈모형,72 h후처사,채용간습질량법측정뇌조직수함량.통계학분석채용Stata 7.0연건진행성조설계자료적t검험.결과 HBOP조대서기저절조직내HO-1단백함량여가예처리상비차이구유통계학의의(P＜0.05);HBOP+ DMSO조대서혈종동측기저절조직수함량위(81.4±0.9)％,현저저우가예처리+ DMSO조(82.6±0.8)％(P＜0.05),단대서접수고압양예처리동시복강내급여HO-1억제제ZnPPⅨ칙저소료HBOP감경뇌출혈후뇌수종적효응[(82.8±0.9)％vs.(82.6±0.7)％(P＞0.05)].결론 고압양예처리현저감경대서뇌출혈후뇌수종,기작용궤제여기상조HO-1단백적표체유관.
Objective To investigate the role of Heme oxygenase-1 in the effect of hyperbaric oxygen preconditioning (HBOP) against the brain edema formation after experimental intracerebral hemorrhage in rats.Methods The study was carried out by animal experiment in two steps by using 54 Spradgue-Dawley rats weighting from 300-350 g.In the first step,rats were treated with HBOP (HBOP group,n =3) or with sham pre-conditioning (Sham pre-conditioning group,n =3).All the rats were sacrificed 24 h after the preconditioning,and basal ganglion of brain tissue was taken for detect HO-1 level by using western blot analysis.In the second step,rats were divided into 4 groups (n =12 in each group):HBOP +ZnPP group,in which rats had a micro-pump intra-peritoneally implanted containing a specific HO-1 inhibitor ZnPPⅨ (Zinc protoporphyrin IX,0.01 mg/kg),Sham pre-conditioning + Znpp group,HBOP + DMSO group,in which rats with a intra-peritoneal micro-pump containing 2 mL Dimethyl sulfoxide (DMSO,a solvent vehicle) and Sham pre-conditioning + DMSO group before HBOP.At 24 hours after the pre-conditioning,rats received an infusion of 100 μL autologous blood into the caudate nucleus to form a simulated intracerebrum hemorrhage (ICH),and were sacrificed 72 h later for brain water content measurements.All data were analyzed by using Stata 7.0 software and statistical analyses were carried out by two-tailed Student t test.Results Compared with the Sham pre-conditioning group,the HBOP group had significant higher level of HO-1.Compared with the Sham pre-conditioning + DMSO group,the HBOP + DMSO group had a significant lower level of water content in the ipsilateral basal ganglion [(81.4 ± 0.9) ％ vs.(82.6 ± 0.8) ％ (P ＜ 0.05)],however,peritoneal infusion of ZnPP Ⅸ before HBOP abolished HBOP-induced protection against brain edema formation after experimental ICH [(82.8 ± 0.9) ％ vs.(82.6 ± 0.7) ％ (P ＞ 0.05)].Conclusions Hyperbaric oxygen preconditioning attenuate brain edema formation after experimental ICH in rats,and this protection is attributed to the activation of HO-1.
