中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2014年
9期
1907-1909
,共3页
孙国柱%杨建凯%赵宗茂%马波涛%朱小辉
孫國柱%楊建凱%趙宗茂%馬波濤%硃小輝
손국주%양건개%조종무%마파도%주소휘
Toll样受体蛋白4%炎性细胞因子%脑损伤%液压冲击
Toll樣受體蛋白4%炎性細胞因子%腦損傷%液壓遲擊
Toll양수체단백4%염성세포인자%뇌손상%액압충격
Toll-like receptor 4%Inflammatory cytokine%Brain injury%Fluid percussion
目的 观察液压冲击脑损伤大鼠Toll样受体蛋白4(TLR4)与炎性细胞因子白细胞介素(IL)-1β、IL-6、肿瘤坏死因子-α(TNF-α)表达变化,探讨TLR4对炎性因子的调控作用.方法 成年雄性SD大鼠48只,制作液压冲击颅脑损伤模型,术后6、12、24 h、3、7d断头处死,用干湿重法、免疫织化法分别测定水肿脑组织含水量及其TLR4、IL-1β、IL-6、TNF-α表达.结果 创伤性颅脑损伤(TBI)组大鼠脑含水量从6h开始增加[(78.86 ±0.54)%],24 h时达到最大值[(83.07±0.27)%],持续至3d开始下降[(81.85±1.26)%];免疫组织化学显示水肿脑组织TLR4、IL-1β、IL-6、TNF-α的表达均在6h时开始增高(1.50±0.58、3.75±0.48、3.50±0.58、5.75 ±2.36),在12h或24 h时达到高峰(5.50±1.00、7.80±1.64、7.75±1.05、7.50±1.73),7d后降低.线性相关分析显示TLR4表达与IL-1β、IL-6、TNF-α表达呈正相关(r=0.941、0.907、0.836,P<0.05).结论 大鼠颅脑液压冲击伤TLR4、IL-1β、IL-6、TNF-α均出现高表达,TLR4可能通过调控炎性因子介导继发性脑损伤.
目的 觀察液壓遲擊腦損傷大鼠Toll樣受體蛋白4(TLR4)與炎性細胞因子白細胞介素(IL)-1β、IL-6、腫瘤壞死因子-α(TNF-α)錶達變化,探討TLR4對炎性因子的調控作用.方法 成年雄性SD大鼠48隻,製作液壓遲擊顱腦損傷模型,術後6、12、24 h、3、7d斷頭處死,用榦濕重法、免疫織化法分彆測定水腫腦組織含水量及其TLR4、IL-1β、IL-6、TNF-α錶達.結果 創傷性顱腦損傷(TBI)組大鼠腦含水量從6h開始增加[(78.86 ±0.54)%],24 h時達到最大值[(83.07±0.27)%],持續至3d開始下降[(81.85±1.26)%];免疫組織化學顯示水腫腦組織TLR4、IL-1β、IL-6、TNF-α的錶達均在6h時開始增高(1.50±0.58、3.75±0.48、3.50±0.58、5.75 ±2.36),在12h或24 h時達到高峰(5.50±1.00、7.80±1.64、7.75±1.05、7.50±1.73),7d後降低.線性相關分析顯示TLR4錶達與IL-1β、IL-6、TNF-α錶達呈正相關(r=0.941、0.907、0.836,P<0.05).結論 大鼠顱腦液壓遲擊傷TLR4、IL-1β、IL-6、TNF-α均齣現高錶達,TLR4可能通過調控炎性因子介導繼髮性腦損傷.
목적 관찰액압충격뇌손상대서Toll양수체단백4(TLR4)여염성세포인자백세포개소(IL)-1β、IL-6、종류배사인자-α(TNF-α)표체변화,탐토TLR4대염성인자적조공작용.방법 성년웅성SD대서48지,제작액압충격로뇌손상모형,술후6、12、24 h、3、7d단두처사,용간습중법、면역직화법분별측정수종뇌조직함수량급기TLR4、IL-1β、IL-6、TNF-α표체.결과 창상성로뇌손상(TBI)조대서뇌함수량종6h개시증가[(78.86 ±0.54)%],24 h시체도최대치[(83.07±0.27)%],지속지3d개시하강[(81.85±1.26)%];면역조직화학현시수종뇌조직TLR4、IL-1β、IL-6、TNF-α적표체균재6h시개시증고(1.50±0.58、3.75±0.48、3.50±0.58、5.75 ±2.36),재12h혹24 h시체도고봉(5.50±1.00、7.80±1.64、7.75±1.05、7.50±1.73),7d후강저.선성상관분석현시TLR4표체여IL-1β、IL-6、TNF-α표체정정상관(r=0.941、0.907、0.836,P<0.05).결론 대서로뇌액압충격상TLR4、IL-1β、IL-6、TNF-α균출현고표체,TLR4가능통과조공염성인자개도계발성뇌손상.
Objective To investigate the expression of Toll-like receptor 4 (TLR4) and inflammatory cytokines such as interleukin (IL)-1β,IL-6 and tumor necrosis factor (TNF)-α,and explore the modulatory effect of TLR4 on inflammatory cytokines following fluid percussion brain injury in rats.Methods The experimental models were established in 48 adult rats.The water content of edematous brain and the expression of TLR4,IL-1β,IL-6 and TNF-α were measured with dry-wet measure,and immunohistochemistry at 6,12,24 h,3 day,and 7 day after operation respectively.Results As compared with shamoperated group,the water content of edematous brain was increased in traumatic brain injury (TBI) group from 6 h [(78.86 ± 0.54) %] to the maximum at 24 h [(83.07 ± 0.27) %],and gradually decreased at 3 day [(81.85 ± 1.26)%].TLR4,IL-6,IL-1β and TNF-α immunoreactive expression was increased from 6 h (1.50 ± 0.58,3.75 ± 0.48,3.50 ± 0.58,and 5.75 ± 2.36 respectively) to the maximum at 12 h or 24 h (5.50 ± 1.00,7.80 ± 1.64,7.75 ± 1.05,and 7.50 ± 1.73 respectively),lasted to the 3rd day,and began to drop at 7th day.The linear regression analysis indicated that TLR4 expression had positive correlations with expression of IL-1 β,IL-6 and TNF-α (r =0.941,r =0.907,r =0.836 respectively,P < 0.05).Conclusion TLR4,IL-6,IL-1β and TNF-α expression is upregulated following fluid percussion injury in rats,and TLR4 is involved in secondary brain injury by mediating inflammatory cytokines.