上海医学
上海醫學
상해의학
SHANGHAI MEDICAL JOURNAL
2009年
12期
1107-1109
,共3页
朱虹%蔡佩佩%王俏%周龙女%朱健
硃虹%蔡珮珮%王俏%週龍女%硃健
주홍%채패패%왕초%주룡녀%주건
高迁移率族蛋白B1%Toll样受体4%脓毒症
高遷移率族蛋白B1%Toll樣受體4%膿毒癥
고천이솔족단백B1%Toll양수체4%농독증
High mobility group protein B1%Toll-like receptor 4%Sepsis
目的 探讨脓毒症大鼠肝组织高迁移率族蛋白B1(HMGB1)和Toll样受体4(TLR4)mRNA的表达变化及其相互关系.方法 采用盲肠结扎穿孔术(CLP)制成脓毒症大鼠模型.将50只Wistar大鼠分成正常对照组(10只)和CLP组(40只),CLP组分别于CLP术后6、12、18、24 h各处死10只大鼠,应用实时聚合酶链反应检测肝脏组织HMGB1和TLR4 mRNA的表达.结果 正常对照组大鼠肝脏组织存在微量的HMGB1、TLR4 mRNA表达.脓毒症组大鼠CLP术后各时间点的HMGB1、TLR4 mRNA表达均显著高于正常对照组(P值均<0.01),CPL术后6 h HMGB1、TLR4 mRNA表达开始升高,至12 h达峰值,18 h后开始下降,各时间点间HMGB1、TLR4 mRNA表达的差异均有统计学意义(P值均<0.05).直线相关分析表明,脓毒症大鼠肝脏组织HMGB1 mRNA与TLR4 mRNA的表达呈正相关(r=0.90,P=0.04).结论 HMGB1可能通过TLR4进一步激活炎性细胞,引起下游炎性因子释放的瀑布效应.
目的 探討膿毒癥大鼠肝組織高遷移率族蛋白B1(HMGB1)和Toll樣受體4(TLR4)mRNA的錶達變化及其相互關繫.方法 採用盲腸結扎穿孔術(CLP)製成膿毒癥大鼠模型.將50隻Wistar大鼠分成正常對照組(10隻)和CLP組(40隻),CLP組分彆于CLP術後6、12、18、24 h各處死10隻大鼠,應用實時聚閤酶鏈反應檢測肝髒組織HMGB1和TLR4 mRNA的錶達.結果 正常對照組大鼠肝髒組織存在微量的HMGB1、TLR4 mRNA錶達.膿毒癥組大鼠CLP術後各時間點的HMGB1、TLR4 mRNA錶達均顯著高于正常對照組(P值均<0.01),CPL術後6 h HMGB1、TLR4 mRNA錶達開始升高,至12 h達峰值,18 h後開始下降,各時間點間HMGB1、TLR4 mRNA錶達的差異均有統計學意義(P值均<0.05).直線相關分析錶明,膿毒癥大鼠肝髒組織HMGB1 mRNA與TLR4 mRNA的錶達呈正相關(r=0.90,P=0.04).結論 HMGB1可能通過TLR4進一步激活炎性細胞,引起下遊炎性因子釋放的瀑佈效應.
목적 탐토농독증대서간조직고천이솔족단백B1(HMGB1)화Toll양수체4(TLR4)mRNA적표체변화급기상호관계.방법 채용맹장결찰천공술(CLP)제성농독증대서모형.장50지Wistar대서분성정상대조조(10지)화CLP조(40지),CLP조분별우CLP술후6、12、18、24 h각처사10지대서,응용실시취합매련반응검측간장조직HMGB1화TLR4 mRNA적표체.결과 정상대조조대서간장조직존재미량적HMGB1、TLR4 mRNA표체.농독증조대서CLP술후각시간점적HMGB1、TLR4 mRNA표체균현저고우정상대조조(P치균<0.01),CPL술후6 h HMGB1、TLR4 mRNA표체개시승고,지12 h체봉치,18 h후개시하강,각시간점간HMGB1、TLR4 mRNA표체적차이균유통계학의의(P치균<0.05).직선상관분석표명,농독증대서간장조직HMGB1 mRNA여TLR4 mRNA적표체정정상관(r=0.90,P=0.04).결론 HMGB1가능통과TLR4진일보격활염성세포,인기하유염성인자석방적폭포효응.
Objective To investigate the changes of high mobility group protein B1 (HMGB1) and Toll-like receptor 4 (TLR4) gene expression in liver of septic rats, and to elucidate the relationship between HMGB1mRNA and TLR4 mRNA expression. Methods Sepsis was induced in rats by cecal ligation puncture (CLP). Fifty Wistar rats were randomly divided into 2 groups: the normal control (n = 10) and the CLP group; the latter was further divided into 6 h, 12 h, 18 h, and 24 h CLP subgroups (n = 10 in each subgroup). The expression of HMGB1 mRNA and TLR4 mRNA in the liver was examined by real-time polymerase chain reaction (PCR). Results Weak expression of HMGB1 mRNA and TLR4 mRNA was observed in the liver of normal rats. The expression levels of both HMGB1 and TIR4 mRNA in the CLP group were significantly higher than those in the normal control group at all time points after operation (P<0.01). The expression of HMGB1 mRNA and TLR4 mRNA increased in 6 h CLP group, peaked in 12 h CLP, and then declined gradually after 18 h, with significant differences found at all time points (P<0.05). Correlation analysis showed that the expression of HMGB1 mRNA was positive correlated with TLR4 mRNA expression in the liver of septic rats (r = 0.90, P = 0.04). Conclusion HMGB1 may further activate inflammatory cells through TLR4, and result in a waterfall effect of the downstream inflammatory factors.